Juliana Morsello Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that impacts how individuals think, learn, and behave (Cleveland Clinic, 2020). Symptoms include difficulties with social interaction, trouble understanding nonverbal communication, and having intense interests. Although we will not be discussing the process of receiving a diagnosis, it is important to note that ASD presents differently depending on the individual, with symptoms varying from “mild to severely disabling.” One factor that can contribute to differences in the neurobiology and presentation of ASD is someone’s sex assigned at birth (Napolitano et al., 2022). However, research on ASD in females remains limited. This gap in understanding, and research on females in general, will be discussed in the following section. In the remainder of this article, we will focus on the neurobiological aspects of sex differences in ASD. It should be noted that I am using the terms “male” and “female” to refer primarily to biological sex and not gender, although future research should continue to investigate differences in ASD related to gender. Underrepresentation of Female Participants in Research  Females are unfortunately disproportionately underrepresented in both general research and clinical trials. This applies not only to human studies but also to nonhuman studies. For example, Beery (2018) reported that only about 20% of neuroscience rat studies include both male and female subjects, and 25% do not specify the sex of the rats at all. Even in studies that include both sexes, it is rare that researchers analyze their results based on sex. Researchers have proposed multiple justifications for the male bias observed in mammal studies. For example, some researchers previously believed that hormonal fluctuations pertaining to female humans and nonhuman female mammals (e.g. menstrual and estrous cycles) would complicate their data collection (Zucker et al., 2021). Additionally, recruiting biases (Merone et al., 2022), personal and practical concerns (e.g. childcare), and religious or cultural norms (Subdeh & Alzoubi, 2021) may also contribute to poor female representation. While underrepresentation is increasingly being addressed by the scientific community, it is equally important to consider the consequences of this phenomenon. For instance, clinicians may fail to diagnose female patients with particular conditions, which can leave them with unresolved treatment needs. Females may also experience adverse reactions to pharmacological treatments that were primarily studied on males (D’Mello et al., 2022). Underrepresentation can have an impact on several research fields. For example, there are typically few female participants in ASD studies, or sometimes male-only samples (D’Mello et al., 2022). This underrepresentation is critical  for us to keep in mind, especially while looking at statistics– According to the CDC, boys are four times more likely than girls to be diagnosed with ASD. If someone interprets this report without any context, they may conclude that ASD is simply more common among males. However, due to a lack of female participants in ASD studies, it is likely that ASD is more evenly prevalent across both sexes, yet there is just a lack of understanding about ASD in females that is deterring the development of more accurate diagnostic criteria. Unfortunately, researchers suggest that flawed diagnostic criteria are a contributing factor in females being undiagnosed, misdiagnosed, or diagnosed with ASD later in life (e.g., Harmens et al., 2022).   Likewise, diagnostic techniques have been shown to exclude females from ASD studies. Researchers in Dr. John Gabrieli’s lab at MIT discovered that the Autism Diagnostic Observation Schedule (ADOS), a common test for determining eligibility for ASD studies, typically screens out more females than males (D’Mello et al., 2022). So, why should this matter? Such exclusion may be limiting our understanding of how ASD affects male and female brains differently, which influences how we define ASD today and the efficacy of treatments for both sexes.  Next, we will discuss just how the neurobiology of ASD differs between males and females, and how these differences can help inform both diagnostic methods and treatment strategies. Brain Development There is evidence to suggest that there are neurodevelopmental sex-differences in the trajectory of ASD. For example, a team of researchers at UC Davis (Andrews et al., 2024) discovered that the brain's cortex thins at different rates in males compared to females with ASD.  Before we discuss Andrews et al.'s (2024) study, it is important to review general patterns of neurodevelopmental differences between sexes. The cortex, the outermost layer of the brain, is made up of gray matter. Gray matter is a type of tissue found in the central nervous system (brain and spinal cord) that processes information and supports higher-level brain functions such as processing sensory information, and controlling emotions, memory, and movement (Cleveland Clinic, 2023). Andrews et al. (2024) investigated sex differences in cortical thickness in children with ASD. “Cortical thickness” is the width of our gray matter, which naturally shrinks as we age. Our cortical thickness increases during the prenatal period, is widest between 1.5-2 years of age, and then begins to thin for the remainder of our lives. Although it has been suggested that individuals with ASD experience different patterns of cortical thickness, this appears to be the first study that has longitudinally examined sex-differences in cortical width in children with ASD.  Andrews et al. (2024) analyzed neuroimaging (MRI) data from the UC Davis Mind Institute ASD Phenome Project (APP). The MRI scans were performed on male and female autistic and non-autistic children aged 3 to 11.5 years. It was found that three-year-old females with ASD had a thicker cortex compared to non-autistic females of the same age. Furthermore, females with ASD began to experience cortical thinning faster during their middle childhood compared to males with ASD.  The researchers suggest that future studies investigate the correlation between cortical structure and changes in ASD symptoms (Andrews et al., 2024) which may not only aid in  improvement of diagnostic criteria, but also result in treatments that are better-tailored to individual needs. It also may give the scientific community more insight into whether sex-specific ASD screening is beneficial, which is a research area that has yielded mixed findings (e.g., Terner et al., 2024; Mårland et al., 2022). In the following sections, we will focus on specific aspects of brain function in autism. Functional Brain Organization  Functional brain organization refers to how different brain regions work together as networks to perform complex functions. In a study by Supekar et al. (2022), an AI algorithm found that brain organization in ASD differs between male and female children (M = 13.2 years). For example, females had different patterns of connectivity than males in language and spatial attention systems. The algorithm was able to distinguish between these patterns in children with ASD, but it could not do the same for neurotypical children, which suggests that these sex-differences are specific to ASD.  Differences in several motor areas, such as the primary motor cortex, were found to be the most important for the algorithm’s ability to predict whether someone is a female with ASD. Interestingly, males with ASD tend to exhibit more repetitive motor behaviors (Karadaş et al., 2021), and in this study, females with similar brain patterns to males had the most prominent motor symptoms. This suggests that females who are autistic, yet just display less apparent repetitive motor behaviors, may be more likely to receive a delayed diagnosis (Digitale, 2022). We will discuss life with a late-life diagnosis in the “Significance” section of this article. Ventromedial Prefrontal Cortex and Camouflaging Another factor that may lead to late-life diagnosis is camouflaging, when individuals with ASD adjust their social behaviors to fit in with their neurotypical peers (Alaghband-rad et al., 2023). In other words, their outward social behavior might differ from how they represent themselves internally/neurologically (self-representation).  In a study by Lai et al. (2018),  researchers examined brain activity in adults with ASD as they performed a task that tested how they see themselves. Using fMRI, the researchers found that males with ASD had a weaker response in a brain area called the ventromedial prefrontal cortex (vmPFC) compared to neurotypical males. Interestingly, for females with ASD, their brain activity in this area was similar to that of neurotypical females. It was also found that females with ASD who camouflaged more had a stronger self-representation response in the vmPFC.  What does this mean? Because females may generally face higher social pressure than males due to traditional sex/gender expectations (Kreiser & White, 2013; as cited in Lai et al., 2018), females with ASD might engage in certain mental processes to help them meet these expectations. This could explain why their activity in the vmPFC is more typical. Additionally, in order to “camouflage successfully,” females with ASD may need to be highly aware of how their own behaviors impact others and align with those of their neurotypical peers, which might explain the positive correlation between camouflaging & vmPFC response (Lai et al., 2018).  An Area for Future Research: The Hippocampal Subareas    A brain region that needs to be further studied in individuals with ASD is the hippocampus. The hippocampus plays a large role in memory, learning, and language, making it an important target for developing ASD treatments (Long et al., 2024). For instance, MRI research has shown that people with ASD have different hippocampal volume compared to neurotypical individuals, which is related to challenges with long-term memory, language skills, social communication, and emotional regulation. However, it is still not fully understood how changes in the hippocampus lead to the cognitive and behavioral challenges seen in ASD.  What is also poorly understood is the function of the hippocampal subareas, whose distinct and overlapping contributions to memory are currently under debate. The subareas include the subiculum, cornu ammonis (CA) 1-3, and dentate gyrus (DG)/C4. Li et al. (2022) chose to research these areas because prior work has shown that children with ASD experience atypical brain overgrowth, but little is known about the development of specific brain regions like the hippocampus. The researchers conducted the first MRI study of the hippocampus subareas in infants with ASD, and found that CA1-3, but not the CA4/DG, showed abnormal increases in size in males at 6, 12, and 24 months of age when compared to neurotypical controls (Li et al., 2022). There were no significant differences found in females in ASD groups and control groups, which may be due to the smaller sample size of females. Additionally, through analyzing brain scans from the National Database for Autism Research (NDAR), the researchers found that CA1-3 overgrowth is followed by excessive reduction during adulthood. However, only males, (6 to 58 years of age) were included in this analysis because the NDAR lacks female subjects (Li et al., 2022). To further address the lack of research on CA1-3 development in ASD, study how atypical changes in these areas manifest both cognitively and behaviorally, and continue research on the hippocampus as a target for ASD treatment, it is crucial that this work is comprehensive, and therefore includes more females. Without this, it will be more challenging for the scientific community to get closer to fully understanding how ASD presentation varies depending on the individual.  Significance  This article mainly discusses the neuroscience of ASD in females. However, I would like to highlight qualitative behavioral studies that shed light on the ASD experience, in an effort to urge the scientific community to conduct more studies with female participants. Through interviews, Milner et al. (2019) provided a platform for females to share their personal experiences living with ASD. Many women made several comments regarding sex/gender: “Every girl has a completely different experience with autism”  “I think it would be nice for people to realize that autism can affect girls”  “Girls are really good at, you know, masking and hiding their autism so that it’s harder to identify an autistic girl that you know needs help with the world”  “Boys are more content to be themselves and it’s like this is how I am, whereas the girls really want to fit in, um, and I think that makes them unhappier”  These comments emphasize the need for more inclusive ASD research. It is not only disheartening to see that females with ASD feel under-recognized, but also that social pressures seem to weigh heavily on their emotional-wellbeing. Ultimately, research on females must continue to be encouraged to help rectify this. While the comments above reflect the impact of camouflaging, some women in Milner et al.'s (2019) sample reported that they find it impossible to camouflage. Perhaps future research in both neuroscience and psychology is necessary to better understand how camouflaging works in both sexes. Impact of Late-Life Diagnosis We previously discussed certain factors that may lead to late-life diagnosis of ASD in females. So why does late-life diagnosis matter? In a study by Stagg and Belcher (2019), researchers found that individuals who received a diagnosis of ASD over the age of 50 felt extremely isolated as children. One woman described her experience with not fitting in, stating, “​​I thought maybe I’m a bad person, I’ve got a horrible personality, there’s something about me people don’t like, and I didn’t understand why.”  When participants finally received a diagnosis later in life, they appeared to have mixed reactions. For example, one woman said, “It really was like a sort of eureka moment … it was kind of a relief … and it wasn’t my fault, and that was one of the biggest things, that I realized it wasn’t my fault.” However, she also mentioned, “It robs me, I guess, of maybe confidence and stuff. Maybe I would have, if I hadn’t got it, I would have maybe done some different things in my life.” While an early diagnosis may not completely eliminate the possibility of feeling isolated, giving someone a sense of knowledge or a label for their experiences might help them better understand themselves and potentially carry greater self-esteem into their adult life. I recognize that individuals who receive a late-life diagnosis may still grapple with unresolved past struggles, and may face stigma or self-doubt due to their new label. Therefore, it is important that research continues on effective ASD support systems, as these systems may help individuals address these challenges.  Concluding Statement While neuroscience research on ASD has made significant strides, it still needs to broaden its scope to include a more diverse range of participants. For instance, beyond sex and gender, historically marginalized racial and ethnic groups remain underrepresented in ASD studies (University of North Carolina, 2022).  Specifically for females with ASD, increasing equal representation across sexes may lead to improved diagnostic criteria and more tailored treatment options. This could not only support individuals with ASD in managing daily challenges but also improve society’s understanding of ASD. By fostering a more empathetic view of ASD, increased inclusivity in research has the potential to promote a more inclusive society that celebrates individuals’ positive experiences with ASD and their unique strengths.  As research advances, we can all increase ASD awareness by educating ourselves and our peers, while also having meaningful conversations with individuals on the autism spectrum to truly understand their experiences. For readers interested in learning more about autism in females and contributing to ASD awareness, I have provided helpful resources below. https://www.autism.org.uk/advice-and-guidance/what-is-autism/autistic-women-and-girls https://www.vanderbilt.edu/autismandinnovation/for-autistic-women/#:~:text=Resources%20for%20Women&text=The%20Asperger%2FAutism%20Network%20(AANE,to%20women%20on%20the%20spectrum. https://behavioral-innovations.com/blog/recognize-autism-awareness-and-what-we-can-learn/#:~:text=Take%20action%20to%20support%20organizations,social%20media%20and%20community%20events . https://autismsociety.org/ways-to-give/ References   Al Subeh, Z. Y., & Alzoubi, K. H. (2021). Researchers’ ethical perspective about women participation in research studies in Jordan. Heliyon , 7 (12), e08492. https://doi.org/10.1016/j.heliyon.2021.e08492 Alaghband-rad, J., Hajikarim-Hamedani, A., & Motamed, M. (2023). Camouflage and masking behavior in adult autism. Frontiers in Psychiatry , 14 (14). https://doi.org/10.3389/fpsyt.2023.1108110 Andrews, D. S., Diers, K., Lee, J. K., Harvey, D. J., Heath, B., Cordero, D., Rogers, S. J., Reuter, M., Solomon, M., Amaral, D. G., & Nordahl, C. W. (2024). Sex differences in trajectories of cortical development in autistic children from 2–13 years of age. Molecular Psychiatry , 1–12. https://doi.org/10.1038/s41380-024-02592-8 Beery, A. K. (2018). Inclusion of females does not increase variability in rodent research studies. Current Opinion in Behavioral Sciences , 23 , 143–149. https://doi.org/10.1016/j.cobeha.2018.06.016 Cleveland Clinic. (2023, March 19). Grey matter . Cleveland Clinic. https://my.clevelandclinic.org/health/body/24831-grey-matter Cleveland clinic. (2020, December 29). Autism Spectrum Disorder (ASD): Causes, Symptoms, Treatment & Outlook . Cleveland Clinic; Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/8855-autism D’Mello, A. M., Frosch, I. R., Li, C. E., Cardinaux, A. L., & Gabrieli, J. D. E. (2022). Exclusion of females in autism research: Empirical evidence for a “leaky” recruitment‐to‐research pipeline. Autism Research , 15 (10). https://doi.org/10.1002/aur.2795 Digitale, E. (2022). Study finds differences between brains of girls, boys with autism . News Center. https://med.stanford.edu/news/all-news/2022/02/autism-brain-sex-differences.html Harmens, M., Sedgewick, F., & Hobson, H. (2022). Autistic women’s diagnostic experiences: Interactions with identity and impacts on well-being. Women’s Health , 18 , 174550572211374. https://doi.org/10.1177/17455057221137477 Karadaş, C., Bakkaloğlu, H., & Demir, Ş. (2021). Exploring the effect of motor coordination on repetitive behaviours in children with autism spectrum disorder. International Journal of Developmental Disabilities , 1–10. https://doi.org/10.1080/20473869.2021.1948318 Kreiser, N. L., & White, S. W. (2013). ASD in Females: Are We Overstating the Gender Difference in Diagnosis? Clinical Child and Family Psychology Review , 17 (1), 67–84. https://doi.org/10.1007/s10567-013-0148-9 Lai, M.-C., Lombardo, M. V., Chakrabarti, B., Ruigrok, A. N., Bullmore, E. T., Suckling, J., Auyeung, B., Happé, F., Szatmari, P., Baron-Cohen, S., Bailey, A. J., Bolton, P. F., Carrington, S., Catani, M., Craig, M. C., Daly, E. M., Deoni, S. C., Ecker, C., Henty, J., & Jezzard, P. (2018). Neural self-representation in autistic women and association with “compensatory camouflaging.” Autism , 23 (5), 1210–1223. https://doi.org/10.1177/1362361318807159 Li, G., Chen, M.-H., Li, G., Wu, D., Lian, C., Sun, Q., Rushmore, R. J., & Wang, L. (2022). Volumetric Analysis of Amygdala and Hippocampal Subfields for Infants with Autism. Journal of Autism and Developmental Disorders . https://doi.org/10.1007/s10803-022-05535-w Long, J., Li, H., Liu, Y., Liao, X., Tang, Z., Han, K., Chen, J., & Zhang, H. (2024). Insights into the structure and function of the hippocampus: implications for the pathophysiology and treatment of autism spectrum disorder. Frontiers in Psychiatry , 15 . https://doi.org/10.3389/fpsyt.2024.1364858 Mårland, C., Nilsson, T., Larsson, H., Gillberg, C., Lubke, G., & Lundström, S. (2022). Measuring autism in males and females with a differential item functioning approach: Results from a nation-wide population-based study. Psychiatry Research , 314 , 114674. https://doi.org/10.1016/j.psychres.2022.114674 Merone, L., Tsey, K., Russell, D., & Nagle, C. (2022). Sex Inequalities in Medical Research: A Systematic Scoping Review of the Literature. Women’s Health Reports , 3 (1), 49–59. https://doi.org/10.1089/whr.2021.0083 Napolitano, A., Schiavi, S., La Rosa, P., Rossi-Espagnet, M. C., Petrillo, S., Bottino, F., Tagliente, E., Longo, D., Lupi, E., Casula, L., Valeri, G., Piemonte, F., Trezza, V., & Vicari, S. (2022). Sex Differences in Autism Spectrum Disorder: Diagnostic, Neurobiological, and Behavioral Features. Frontiers in Psychiatry , 13 . https://doi.org/10.3389/fpsyt.2022.889636 Stagg, S. D., & Belcher, H. (2019). Living with autism without knowing: receiving a diagnosis in later life. Health Psychology and Behavioral Medicine , 7 (1), 348–361. https://doi.org/10.1080/21642850.2019.1684920 Supekar, K., Angeles, C. de los, Ryali, S., Cao, K., Ma, T., & Menon, V. (2022). Deep learning identifies robust gender differences in functional brain organization and their dissociable links to clinical symptoms in autism. The British Journal of Psychiatry , 1–8. https://doi.org/10.1192/bjp.2022.13 Terner, M., Israel-Yaacov, S., & Golan, O. (2024). Sex differences in autism screening: An examination of the Childhood Autism Spectrum Test–Hebrew version. Autism . https://doi.org/10.1177/13623613241235053 The University of North Carolina at Chapel Hill. (2022). Study shows lack of representation across historically minoritized racial and ethnic groups in autism intervention data | Frank Porter Graham Child Development Institute . Fpg.unc.edu . https://fpg.unc.edu/news/study-shows-lack-representation-across-historically-minoritized-racial-and-ethnic-groups-autism#:~:text=White%20participants%20made%20up%2064 Zucker, I., Prendergast, B. J., & Beery, A. K. (2021). Pervasive Neglect of Sex Differences in Biomedical Research. Cold Spring Harbor Perspectives in Biology , a039156. https://doi.org/10.1101/cshperspect.a039156

Olivia Gudeahn Libraries are loud . Children playing, pages turning, keyboards typing, and lively chatter are all vibrant sounds at the library. Libraries aren’t just a place for silent reading and shushing librarians, but a place where community grows. How do I know all this?  I’ve spent the last three summers working at my hometown library as a circulation desk clerk and a programming assistant. Throughout working at my library, I’ve met many community members and gotten to know a bit about their experiences. I also have a first hand look at the resources patrons find helpful. In 2017, “More than 172 million registered users, representing 55% of the 312 million Americans who lived within a public library service area, visited public libraries 1.32 billion times in 2017. In other words, on average, each American visited a public library over 4 times,” (Institute of Museum and Library Services, 2020). Public libraries offer many services beyond promoting literacy- they offer locations to use Wi-Fi, computer usage, printing services, programming, research assistance, and many more services. Libraries provide a safe space for individuals, and patrons can rest assured that “Neither federal agents nor police officers are legally authorized to demand library records without first providing some form of judicial process (subpoena, search warrant, or other legally enforceable court order) to the library holding the records,” (American Library Association, 2021). This level of privacy and security provides comfort for those who decide to check out materials on sensitive topics. and knowing that their check-out history is secure provides an extra sense of safety. Bibliotherapy Bibliotherapy is  “the act of reading a book to aid a mental illness,” (McCaffrey, 2016). While bibliotherapy doesn’t claim to be a replacement for traditional counseling, it has absolutely been shown to have benefits of its own. In controlled psychological studies, bibliotherapy has been found to aid a wide range of age groups, from young children and adolescents, to adults and parents.  Studies using bibliotherapy showed it improved aggression in young boys, reduced fear of the dark in children, benefited mild to moderately depressed adolescents, and aided parents in improving the behavior of their children (McCaffrey, 2016).  Bibliotherapy has three main tenets: identification, catharsis, and problem solving/insight (Allen et al., 2012; American Library Association, 2015). A person will see themselves in a character and go through the story together. Catharsis happens when the story concludes and tension experienced along the way dissipates. The person can connect their experiences with the character and relate to how the character’s completed arc, thus resulting in problem solving/insight. Together, these tenets create bibliotherapy. Bibliotherapy commonly uses self-help books to facilitate treatment, while creative bibliotherapy utilizes fiction books in treatment (Redman et al., 2024). The word library  means “place for books,” (Online Etymology Dictionary, 2017), which is perhaps what libraries are best known for. Rows and rows of books of every genre are available to the public. How can a simple book help a patron’s mental health? Spending just 6 minutes reading a book can reduce stress levels by 68% (Roff Farrar, 2021). When bibliotherapy takes place at a library, people can reap extra benefits. A library provides a safe and calm environment, and for children, “reinforcement of related assumptions such as, adults can soothe and help and that there is goodness in the world,” (Allen et al., 2012). Reading and listening to stories can provide a calming distraction for people in crisis.  The Unhoused Population As mentioned before, libraries are more than just places for books. During my time as a library employee, I’ve helped many patrons with their requests. A man who didn’t have a GPS and needed a map, a woman who needed to email a PDF, a man who needed access to a database, are just some patrons I’ve helped. Libraries do not discriminate against patrons for any reasons; anyone is welcome in a library. My local library has seen an increase in unhoused patrons over the years. Post-pandemic, “libraries across the US are increasingly on the frontlines of America’s homelessness crisis,” (Ryan, 2023). Among the unhoused population, 67% have a mental illness (Harris, 2024).  Some libraries are implementing Homeless Training, a program that aims to teach deescalation tactics to librarians and staff members. Ryan Dowd of Homeless Training remarks “‘libraries are everything homelessness is not’”, and, “‘It’s a public space, for communal use. If the option is that or be outside all day in 15-degree weather, I know what I’d do,’” (Ryan, 2023). Often, unhoused people will walk to the library and make use of the computers and other resources available (Ryan, 2023). Libraries are a great place for unhoused patrons to conduct research into employment and mental health care. While access to a library may not solve every problem an unhoused patron faces, it can be a great place to begin.  Literacy After the COVID-19 pandemic, literacy rates in children decreased globally. The “disruption to education has meant millions of children have significantly missed out on the academic learning they would have acquired if they had been in the classroom, with younger and more marginalized children facing the greatest loss,” (Unicef, 2022). Consequences of low literacy rates include a “limited ability to obtain and understand essential information, low self esteem, increased rate of workplace accidents, lower quality jobs, and reduced access to lifelong learning,” (Literacy Pittsburgh, n.d.). Libraries can combat the decrease in literacy by having early-literacy programs. Many public libraries offer storytimes – an interactive and educational environment for young children – which are “now viewed as a critical component of young children’s preparation to enter school. They are also vehicles for giving parents guidance on how to encourage early literacy skills at home,” (UWA, 2020).  Libraries also provide a literacy-rich environment for patrons of all ages to utilize. Many libraries offer assistance to “English language learners (ELLs) and students in English as a Second Language (ESL) programs,” (U.S. Citizenship and Immigration Services, n.d.). As of 2024, 14% or 32 million U.S. adults are functionally illiterate and “46% of American adults cannot understand basic financial documents like balance sheets and income statements,” (Bright Futures, 2024). Adults who are functionally illiterate have been found to have higher instances of mental health issues (Zhang, 2020). Another consequence of functional illiteracy is lower levels of health literacy. Health literacy is “the personal characteristics and social resources needed for people to access, understand and use information to make decisions about their health,” (Zhang, 2020). Libraries play an active role in educating learners of all ages and working to combat the literacy crisis. It is crucial for literacy resources to be available in as many communities as possible. Additionally, “more than 370 million children globally missed out on school meals during school closures, losing what is for some children the only reliable source of food and daily nutrition,” (Unicef, 2022). In New York State, 60 public libraries provide lunches to children over the summer (Resources: Summer Reading at New York Libraries: Summer Meals Program, 2023). Hunger is detrimental to healthy development; it is critical for children to receive necessary nutrition. During the summer, “41% of parents struggle in some way to provide food when school is closed, and that nearly half (44%) of parents are more worried now than they were this time last year about getting their kids fed,” (Greenfield, 2024). It is evident that summer hunger is a problem in the United States. However, libraries can work with local resources and grants to provide nutrition over the summer.  Final Reflection Libraries are no longer the home of grumpy librarians. In the modern era, libraries provide resources to all patrons regardless of societal or economic status. They provide essential resources such as access to technology, enhancing education, and provide a community for personal and professional development. Watching the library change into a modern role has been a fascinating experience. I think as the world continues to develop, the library will continue to take on a modern role as a pillar of community. References Allen, J. R., Allen, S. F., Latrobe, K. H., Brand, M., Pfefferbaum, B., Elledge, B., Burton, T., & Guffey, M. (2012). The power of story. The Journal of the Association for Library Service to Children , 10 (1). American Library Association. (2015). Bibliotherapy . Ala.org . https://www.ala.org/tools/atoz/bibliotherapy#:~:text=Ideally%2C%20the%20process%20occurs%20in American Library Association. (2021, October). Law Enforcement Inquiries - Key Concepts . Ala.org . https://www.ala.org/advocacy/privacy/lawenforcement/inquiries#:~:text=Check%20to%20see%20if%20your Bright Futures. (2024, June 5). 22+ US Literacy Statistics: Literacy Rate, Average Reading Level . Www.brightfuturesny.com . https://www.brightfuturesny.com/post/us-literacy-statistics#:~:text=Top%20U.S.%20Literacy%20Rate%20Statistics Greenfield, B. (2024, June 20). Here’s why America’s kids are going hungry over the summer . Fortune Well. https://fortune.com/well/article/americas-kids-hungry-over-summer/ Harris, E. (2024). Two-Thirds of Unhoused People Have Mental Health Disorders. JAMA , 331 (21), 1795–1795. https://doi.org/10.1001/jama.2024.7725 Institute of Museum and Library Services. (2020, July 16). People Visited Public Libraries More Than a Billion Times in One Year . Www.imls.gov . https://www.imls.gov/news/people-visited-public-libraries-more-billion-times-one-year Knapp, A., Hersch, E., Wijaya, C., Herrera, M., Kruzan, K., Carroll, A., Simmons, R., Sodhi, D. K., Hannah, N., Reddy, M., Karnik, N., Smith, J., Brown, C. H., & Mohr, D. (2023). “The library is so much more than books”: considerations for the design and implementation of teen digital mental health services in public libraries. Front. Digit. Health , 5 , 1183319. https://doi.org/10.3389/fdgth.2023.1183319 Literacy Pittsburgh. (n.d.). The Challenge | Causes of Low Literacy . Literacy Pittsburgh. https://www.literacypittsburgh.org/the-challenge/#:~:text=For%20individuals&text=Impact%20on%20health%3A%20low%20literacy McCaffrey, K. (2016). Bibliotherapy: How Public Libraries can Support their Communities’ Mental Health. Dalhousie Journal of Interdisciplinary Management , 12 (1). https://doi.org/10.5931/djim.v12i1.6452 Online Etymology Dictionary. (2017, September 28). library | Etymology, origin and meaning of library by etymonline . Www.etymonline.com . https://www.etymonline.com/word/library Redman, H., Melendez-Torres, G. J., Bethel, A., & Green, J. (2024). The impact of school-based creative bibliotherapy interventions on child and adolescent mental health: a systematic review and realist synthesis protocol. Systematic Reviews , 13 (1). https://doi.org/10.1186/s13643-024-02482-8 Resources: Summer Reading at New York Libraries: Summer Meals Program . (2023). Libguides.com . https://nyslibrary.libguides.com/c.php?g=1284706&p=9432928 Roff Farrar, A. (2021, May 10). Novels and neurons: the very real science of bibliotherapy and the fascinating ways that reading can change our brains for the better . Www.panmacmillan.com . https://www.panmacmillan.com/blogs/lifestyle-wellbeing/mental-health-benefits-reading-bibliotherapy Ryan, M. (2023, January 24). Why US libraries are on the frontlines of the homelessness crisis . The Guardian. https://www.theguardian.com/us-news/2023/jan/24/us-libraries-homeless-crisis-social-workers Stringer, H. (2020, April 1). Libraries as mental health hubs. Https://Www.apa.org . https://www.apa.org/monitor/2020/04/libraries-health-hubs Thomas, S., & Lovelace, K. (2019). Combining efforts: Libraries as mental health safe spaces Combining efforts: Libraries as mental health safe spaces . https://mds.marshall.edu/cgi/viewcontent.cgi?article=1068&context=lib_faculty U.S. Citizenship and Immigration Services. (n.d.). Assisting English Language Learners in Your Library . https://www.uscis.gov/sites/default/files/document/guides/Assisting_ELLs.pdf Unicef. (2022, January 24). COVID:19 Scale of education loss “nearly insurmountable”, warns UNICEF . Www.unicef.org . https://www.unicef.org/eap/press-releases/covid19-scale-education-loss-nearly-insurmountable-warns-unicef UWA. (2020, October 21). Library Storytime Remains Important for Student Learning | UWA . UWA Online. https://online.uwa.edu/news/library-storytime-important-student-learning/ Zhang, Q. (2020). The cost of illiteracy: A causal inference study on how illiteracy affects physical and mental health. Health Education Journal , 80 (1), 54–66. https://doi.org/10.1177/0017896920949894

By: Bernd van Ruremonde Introduction Mary Shelley’s Frankenstein  is a novel known by many and widely adopted into popular culture. The tale is about doctor Victor Frankenstein, a man who is captivated by the force of life. He aims to recreate this force by forming his own sentient life, sewing together dead body parts and imbuing it with lightning, wherafter it springs to life. While the story is fictional, many aspects of it are getting closer to our reality due to many scientists on the quest to build an artificial consciousness. Fundamentally, these scientists are attempting the same as Victor: creating intelligent life. Science, however, is focused on the ‘intelligent’ part. The internet has been full of it lately: Generative Artificial Intelligence, often simply referred to as AI. The rise of OpenAI’s ChatGPT  has flipped a large part of the world upside down, with policymakers scrambling to form new laws around Generative AI. And yet, AI is increasingly becoming a buzzword, with old technologies just getting the ‘AI’ label slapped on to sound more modern. So what really is AI? And why are so many people afraid of it? Background Firstly, there is an important distinction to be made. AI can be classified as ‘strong’ or ‘weak’ (Searle, 1980). Now,  this isn’t a distinction made on the basis of computing power, but more about the fundamental idea behind it. ‘Strong’ AI has the goal of understanding the human mind as a computational device, and possibly recreating it. ‘Weak’ AI, on the other hand, is simply the practice of developing intelligent machinery or software that solves problems (Liu, 2021). While the difference might seem slight, both types approach the field from the exact opposite sides. Alan Turing, famous for his work in cracking the Nazi’s Enigma  cypher, and for his great contributions to the field of computer science, was one of the first people to approach AI from the strong side. Until then, most researchers were focused on building rigid but powerful machines, Turing proposed the concept of a ‘Child Machine’ - an unorganized, simple system based on networks between simple nodes that would learn and develop intelligence like a human child (Sterrett, 2012). This concept would later develop into what we now know as neural networks. Turing (1950) also developed a thought experiment: the Imitation Game, now better known as the Turing test. The Imitation Game’s purpose was to discern when an AI was sentient. The idea behind the test was that there are three agents: a human evaluator and two partners, one being a computer program. The partners will then talk to the evaluator and if the evaluator can’t with certainty tell which one is the human and which one is AI, the AI would ‘pass’ the game and be considered intelligent. Nowadays, the Turing test isn’t seen as very reliable. ChatGPT , for example, has demonstrated the ability to pass the test (Biever, 2023), and experts agree that the chatbot is not intelligent nor conscious (He et al., 2023). But Turing’s ‘Child Machine’ did catch on: neural networks are fundamentally the same. When did the neuron turn into a node? Before we delve into this, let me quickly give you some definitions: a neuron  refers to a biological nerve cell that transmits, generates or receives information in the form of electrical or chemical signals, usually found in the central and peripheral nervous systems. A node  refers to an artificial interpretation of a neuron, usually represented by a complex mathematical formula that decides when the node is activated (a sigmoid function, for those interested). A neural network  is a combination of a large number of nodes, which work together to accomplish a certain task prescribed by the designer. The first idea of a neural network came in 1958, from psychologist Frank Rosenblatt. He wanted to know how information was acquired, stored, and how it affected behavior. With these questions in mind, Rosenblatt (1958) proposed the Perceptron , different nodes linked together in order to ‘sense’. The original perceptron was rudimentary and a proof of concept, but it quickly evolved into something known as a multi-layer perceptron. In a multi-layer perceptron (MLP), many of these nodes are stacked on top of each other to form a layer, and these layers are again stacked to form the perceptron. The multi-layer perceptron is also known as a neural network. Each node from one layer is connected to each node from the layer before and the layer after, and the strength (or more officially, ‘weight’) of these connections is dependent on the information that has passed through the system. Automatically adjusting these weights based on labeled input is what we know as learning, but is formally called training (hence “training a machine learning model”). Even though these perceptrons have significantly improved over time, they still do not even come close to the complexity of a biological neuron. In fact, David Beniaguev (2021) and his team found that to accurately represent the full complexity of a single biological neuron, they needed a deep neural network (DNN) consisting of five to eight layers, each of which consisted of 128 nodes. That’s between 640 and 1024 nodes just to mimic the complexity of one neuron! Now consider that the human brain has, on average, 86 billion neurons. So, the next time you are wondering why we haven’t built a full reconstruction of the human brain digitally, remember that it would take more than 70 trillion artificial nodes. Conclusion Both our knowledge of the human brain and our computing capabilities have greatly improved over the past decades. We are currently in an AI boom, and it is likely that in the near future we will look back at the place we are now the same way we look back at Turing and Rosenblatt. While it might feel like we are far away from a true artificial intelligence, the systems we have now come quite close to it. And though the foundations are still the same, the multi-layer perceptron has evolved far from the original perceptron that Rosenblatt proposed in 1958. Bibliography & Further Reading Beniaguev, D., Segev, I., & London, M. (2021). Single cortical neurons as deep artificial neural networks. Neuron , 109 (17), 2727-2739.e3. https://doi.org/10.1016/j.neuron.2021.07.002   Biever, C. (2023). ChatGPT broke the Turing test — the race is on for new ways to assess AI. Nature , 619 (7971), 686–689. https://doi.org/10.1038/d41586-023-02361-7   He, Q., Geng, H., Yang, Y., & Zhao, J. (2023). Does ChatGPT have consciousness? Brain‐X , 1 (4). https://doi.org/10.1002/brx2.51   Liu, B. (2021). “Weak AI” is Likely to Never Become “Strong AI”, So What is its Greatest Value for us? ResearchGate . https://www.researchgate.net/publication/350484538_Weak_AI_is_Likely_to_Never_Become_Strong_AI_So_What_is_its_Greatest_Value_for_us   Rosenblatt, F. (1958). The perceptron: A probabilistic model for information storage and organization in the brain. Psychological Review , 65 (6), 386–408. https://doi.org/10.1037/h0042519   Searle, J. (1980). The Chinese room experiment . https://rintintin.colorado.edu/~vancecd/phil201/Searle.pdf   Sterrett, S. G. (2012). Bringing up Turing’s ‘Child-Machine.’ In Lecture notes in computer science  (pp. 703–713). https://doi.org/10.1007/978-3-642-30870-3_71   Turing, A. M. (1950). I.—COMPUTING MACHINERY AND INTELLIGENCE. Mind , LIX (236), 433–460. https://doi.org/10.1093/mind/lix.236.433

By: Kate Leinenweber Brain atrophy and differences in cells between a healthy brain and a brain with Alzheimer’s disease. Image created in BioRender. The Mayo Clinic estimates that, after being diagnosed with Alzheimer’s disease, patients can live from 3-11 years, with some even living for 20. Although there are many possible reasons behind this variation – from how far the disease has progressed by the time of diagnosis, to the quality of care that the person with Alzheimer’s receives – one major factor in disease progression is biological. Every person’s body is primed differently to deal with Alzheimer’s disease due to their genetics, lifestyle, and age. However, in a scientific era where genomics have the spotlight, the cellular mechanisms behind Alzheimer’s and the genes that contribute to them are particularly under scrutiny. What biological factors make the disease progress at different speeds for different people, and what does that tell us about how we can go about treating it? In recent studies, the immune system has been shown to play a role in Alzheimer’s disease, possibly slowing disease onset and progression (Pereira, 2022). A type of cell present in the brain, called microglia, are responsible for regulating the immune response in the central nervous system. Microglia are macrophages, meaning that they are immune cells which engulf (or, literally, eat) anything in the body that shouldn’t be there. Macrophages in the rest of our body get rid of pathogens like bacteria and viruses before they can infect us; microglia get rid of debris and monitor damaged neurons or synapses to keep our brains functioning at their best. In Alzheimer’s disease, dead neurons and debris that accumulate in the brain contribute to worsening disease symptoms. By preventing the accumulation of debris in the brain, microglia are able to prevent Alzheimer’s symptoms from progressing as quickly as they would otherwise. Amyloid and Tau Protein in Alzheimer’s Biologically, Alzheimer’s disease is characterized by the aggregation of misfolded proteins in the brain, called amyloid plaques and tau neurofibrillary tangles. The presence of these abnormal proteins is not just a possible indicator of the disease; it is what doctors have been actively using to diagnose Alzheimer’s in recent years (Jack, 2024). Amyloid and tau are widely accepted to be a part of Alzheimer’s disease, and PET scans of Alzheimer’s patients generally show that both of these proteins – especially their misfolded or otherwise abnormal versions – are present in much higher amounts compared to healthy patients. Recent research has also shown that certain molecules which indicate inflammation in the body are present in higher amounts for Alzheimer’s patients (Jack, 2024). In addition to this, certain genes associated with the inflammatory response, such as the TREM2 gene, have variants that are correlated with a higher likelihood of developing Alzheimer’s. In one study, a rare mutated version of TREM2 was associated with nearly 3 times the risk and 3 years earlier onset of Alzheimer’s, further indicating that the immune system is involved in the disease’s progression (Jonnson, 2013). Neuroinflammation The state of the immune system has been shown to change throughout the stages of Alzheimer’s in various ways. The most well known part of the immune response to Alzheimer’s is what occurs near the beginning of disease onset: in a process called neuroinflammation, the brain reacts to the presence of molecules like amyloid and tau by instigating a reaction from the immune system. Dying neurons also release signal molecules called DAMPs, which alert our microglial cells that something is going wrong around them (Wu, 2021). Microglia are then activated and begin to engulf amyloid and tau proteins, as well as debris from dead neurons. Microglia have been a recent focal point of Alzheimer’s research due to their increasingly clear role in the brain’s inflammatory response to the disease, as well as how their activity can help slow disease progression. Initially, microglia are protective against Alzheimer’s disease progression because they clear up amyloid plaques and other aggregated proteins (Pereira, 2022). However, the constant accumulation of protein aggregates leads to chronic microglial activation and therefore chronic neuroinflammation. Due to this process, microglia in later stages of Alzheimer’s become ineffective at their job and can even promote faster disease progression. Microglia tend to exhibit this detrimental behavior near the late stages of Alzheimer’s disease, when amyloid plaques and tau tangles are so numerous and neuron death is so widespread that their activity is no longer preventative. Chronic inflammation can even cause extra damage to the brain, making the later stages of the disease get worse faster. Researching New AD Treatments Information like this can seem unhelpful or hopeless – after all, what can we do if our own cells cannot continuously combat Alzheimer’s progression? Learning things like this can be scary, but it can also provide hope. Everything that teaches us more about Alzheimer’s disease and the workings behind it also teaches us more about how we can research and treat the disease. We know that the immune system and the inflammatory response are involved in the progression of Alzheimer’s, and that the most obvious mechanism of this is that microglia clear up debris that accumulates in the brain. We also know that there are certain genes that increase the risk of Alzheimer’s, but it is not always clear how these are related to each other. For example, the APOE gene is so highly associated with late-onset Alzheimer’s that there is genetic testing available to see if people carry a mutation that puts them at risk ( Fortea, 2024) . The TREM2  gene, which codes for a protein involved in microglia activation, also has variants that increase Alzheimer’s risk, which were correlated with both earlier onset and faster disease progression (Jonsson et. al., 2013).  The more we learn about genes like this through genomic profiling, cell culture, PET scans, and other scientific endeavors, the more we will be able to understand the intricacies of the immune response’s role in Alzheimer’s disease. In the near future, treatments may begin targeting both amyloid/tau accumulation and inflammatory modulators like TREM2, hopefully providing more specific and effective Alzheimer’s medication. References Fortea, J., Pegueroles, J., Alcolea, D. et al.   APOE4  homozygosity represents a distinct genetic form of Alzheimer’s disease. Nat Med  30, 1284–1291 (2024). https://doi.org/10.1038/s41591-024-02931-w . Jack Jr. C.R., Andrews J.S., et. al. Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association 20(8), 5143-5169 (2024). https://doi.org/10.1002/alz.13859 . Johnsonn, T.., Stefansson, H., et. al. Variant of TREM2 Associated with the Risk of Alzheimer's Disease. New England Journal of Medicine 368, 107-116 (2013). https://doi.org/10.1056/NEJMoa1211103 . Leng, F., Edison, P. Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?. Nat Rev Neurol  17, 157–172 (2021). https://doi.org/10.1038/s41582-020-00435-y Mayo Clinic Staff. Alzheimer's stages: How the disease progresses. Mayo Clinic (2023). https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448 Pereira, J.B., Janelidze, S., Strandberg, O. et al.  Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer’s disease pathology. Nat Aging  2, 1138–1144 (2022). https://doi.org/10.1038/s43587-022-00310-z . Woodburn, S.C., Bollinger, J.L. & Wohleb, E.S. The semantics of microglia activation: neuroinflammation, homeostasis, and stress. J Neuroinflammation  18, 258 (2021). https://doi.org/10.1186/s12974-021-02309-6 . Wu, K.M., Zhang, Y.R., et. al. The role of the immune system in Alzheimer’s disease. Ageing Research Reviews 70, (2021). https://doi.org/10.1016/j.arr.2021.101409 .

Written by: Elizabeth Aliyeva; Edited by: Mia Rakotobe-Joely Picture a room full of enthusiastic, 10-year-old students, each with a tablet containing the game "Ethics Quest." This simulation, more than just a game, lets players explore a world full of moral dilemmas and ethical challenges. Students are faced with the first of many from the start: Their virtual village has limited resources, and they have to determine how to distribute food, water, and medicine to the villagers. Should they focus on the older generation with wisdom and experience or the younger villagers who symbolize the future? With every decision made, the children face more and more difficult moral dilemmas, such as deciding whether to assist a stranger despite potential danger or deciding whether to punish a villager who stole to provide for their family. One student is deeply engrossed in the game. At a certain stage, each student must choose whether to reveal the truth behind a friend's error, leading to consequences but potentially facilitating the friend in gaining valuable insight. While considering their choices, they start to feel the gravity of their decisions, understanding that there are no definite correct or incorrect solutions, just different nuances of gray. Following the game, the teacher starts a conversation about the choices the students made and the reasons behind them. While the children converse, it is clear that the game has prompted them to face challenging moral dilemmas and contemplate their own principles and convictions, not just entertain them. One student poses a question to the class: "Is it better to consistently tell the truth, or should we occasionally fib to spare someone's emotions?" Another person questions, "What if being honest could prevent someone from repeating the same error?" The discussion broadens to include a philosophical debate on morality. The students are considering if the decisions they make in the game reflect their real-life choices, and if the ethical values they use online are the same as those they have in real life. They investigate the idea of moral relativism, debating whether ethical principles are universal or contingent on circumstances and viewpoints. In "Ethics Quest," young minds are not only discovering ethics but also delving into the profound philosophical query:  Do our decisions in virtual realms represent our authentic selves, or do they unveil a different facet of our moral personality that may remain hidden in reality? Moral relativism is the philosophical view that moral judgments and values are not absolute but are relative to the cultural, societal, or individual perspectives from which they originate. According to moral relativism, what is considered morally right or wrong can vary from one culture or individual to another, and there is no universal standard that applies to all people at all times. There are different forms of moral relativism, but two of the most common are: Cultural Relativism:  This form of moral relativism suggests that moral beliefs and practices are grounded in and shaped by cultural contexts. According to cultural relativism, what is considered morally right in one culture might be seen as wrong in another. For example, a practice deemed acceptable in one society might be unacceptable in another, and each society's moral code is considered valid within its context. Individual Relativism : This form of moral relativism posits that moral judgments are based on personal beliefs and feelings. According to individual relativism, each person has their own moral framework, and moral judgments are true or valid relative to that individual's perspective. In this view, moral truth is subjective and varies from person to person. When discussing video games, moral relativism provides a perspective to analyze how the moral reasoning of players is affected and mirrored by interactive digital settings. Video games frequently pose intricate ethical dilemmas and a variety of moral situations for players to navigate, prompting them to make choices that mirror their own personal or cultural beliefs. From a psychological perspective, these gaming experiences can show how moral relativism appears in virtual environments. Gamers can choose from various moral codes in a game, making decisions based on their personal beliefs and the cultural settings presented in the game. Decisions in games can reflect actual moral thought processes, showing how personal and cultural influences impact ethical perspectives.  Several studies investigating the relationship between video games and moral development can be connected to the concept of moral relativism, which suggests that moral beliefs and judgments vary based on individual perspectives and cultural contexts. In the study conducted by Hodge et al., the lack of a clear link between video game play and moral development among university students highlights how moral reasoning might be shaped by diverse influences beyond just gaming. For instance, the study observed that males had higher moral scores than females and found different patterns of video game use among players (Hodge et al., 2020). These variations, much like moral relativism, suggest that moral development is influenced by a range of factors, including personal and cultural contexts. The differences in how individuals engage with video games—such as the types of games they play and their gaming habits—reflect how personal experiences and societal norms shape moral understanding (Hodge et al., 2020). This aligns with moral relativism’s view that morality isn’t absolute but varies across different contexts and perspectives. In essence, the study illustrates that moral development might be influenced by individual and cultural factors, rather than a direct cause-and-effect relationship with video game play. This supports the notion of moral relativism, showing that moral beliefs and reasoning can be diverse and shaped by a variety of influences, including how one interacts with and interprets media like video games. Continuing, Pryzybylski’s (2012) study on video games and ideal self-concepts can be related to moral relativism by considering how personal and cultural contexts shape players' experiences and motivations. In this study, the researchers found that players are motivated to engage with video games when these games allow them to experience aspects of their ideal selves (Pryzybylski et al., 2012). It becomes evident that personal self-concepts, guided by the individual desires and cultural norms that encompass moral relativism, impact how people interact with media. The enjoyment and emotional impact of video games are thus influenced by players' personal and cultural contexts, reflecting their unique values and ideals. Just as moral relativism acknowledges that moral standards vary across different contexts, the study shows that video game appeal and emotional responses are also shaped by players' personal perceptions and aspirations (Pryzybylski et al., 2012). Games that resonate with players' ideal selves provide a personalized experience, reinforcing the idea that moral and emotional responses are not universal but are instead influenced by individual and cultural contexts. Wagener & Melzer’s (2024) study on violent video games (VVGs) and moral distress illustrate key aspects of moral relativism. For instance, individuals with higher Dark Tetrad (DT) traits, such as narcissism or psychopathy, experienced less moral distress from violent media (Wagener & Melzer, 2024). This aligns with moral relativism, as these individuals may have different moral standards or be less sensitive to moral transgressions due to their personality traits. Their personal or cultural norms might render the depiction of violence less troubling compared to others who might have stricter moral frameworks. Moreover, moral relativism posits that moral judgments can vary significantly based on cultural and situational contexts. Wagener & Melzer’s (2024) finding that even mild violence can trigger moral distress suggests that what is considered morally troubling can differ widely. This variability reflects how personal or cultural norms influence perceptions of moral issues, supporting the idea that moral distress is not universal but context-dependent. The concept of desensitization, where repeated exposure to violence reduces emotional responses, further illustrates moral relativism. As individuals become more accustomed to violence in the media, their moral standards might shift, making them less sensitive to such content. This evolving perception underscores how personal experience and repeated exposure can influence moral judgments. Finally, Wagener & Melzer’s (2024) results imply that personality traits significantly impact moral distress from media violence. People with certain traits, such as higher DT expressions, might be less affected by violent content (Wagener & Melzer, 2024). This aligns with moral relativism’s view that moral judgments are subjective and shaped by individual characteristics and experiences.  Video games have evolved into a highly influential medium in modern society, captivating millions with their immersive experiences and interactive narratives. From a psychological standpoint, video games represent a double-edged sword when it comes to ethics and morality. On one hand, they offer unique opportunities for moral development and self-exploration. They allow players to engage with complex ethical dilemmas, simulate moral reasoning, and experience consequences for their virtual actions. Games with rich narratives and moral choices can potentially foster empathy and reflection, making them a powerful tool for exploring and understanding diverse perspectives. However, this potential is tempered by the risks associated with video game content, particularly when it comes to violent or morally ambiguous scenarios. Research has shown that exposure to violent video games can induce moral distress, especially when the content clashes with a player’s ethical values. This distress can be mitigated or exacerbated by individual differences such as personality traits or gaming experience. For instance, players with higher levels of moral disengagement or certain personality traits may experience less moral distress, potentially leading to a desensitization to violence and a shift in moral standards. This dual effect illustrates how video games can both challenge and reinforce existing moral frameworks. References Gary Lee Wagener, & Melzer, A. (2024). Game Violence and Moral Distress. Journal of Media Psychology . https://doi.org/10.1027/1864-1105/a000428 Hodge, S. E., Taylor, J., & McAlaney, J. (2020). Is It Still Double Edged? Not for University Students’ Development of Moral Reasoning and Video Game Play. Frontiers in Psychology , 11 . https://doi.org/10.3389/fpsyg.2020.01313 Przybylski, A. K., Weinstein, N., Murayama, K., Lynch, M. F., & Ryan, R. M. (2012). The ideal self at play: the appeal of video games that let you be all you can be. Psychological Science , 23 (1), 69–76. https://doi.org/10.1177/0956797611418676 Yount, D. (n.d.). INDIVIDUAL AND CULTURAL RELATIVISM . https://resources.saylor.org/wwwresources/archived/site/wp-content/uploads/2012/02/BUS205-11.2.1-Individual-and-Cultural-Relativism.pdf

By Gabriella Martinez COVID-19’s impact persists beyond the initial infection, with post-COVID syndrome (PCS, also known as Long COVID) affecting 10-20% of those infected (World Health Organization, 2022). The Centers for Disease Control Prevention  (2024) define PCS as a chronic illness caused by COVID-19 that presents with symptoms for at least three months after a COVID-19 infection, impacting multiple organ systems. One of the most common symptoms, brain fog, is raising serious concerns about cognitive impairments in those living with Long COVID. This article will be exploring possible mechanisms that cause PCS-related brain fog as a way to spark conversation and generate interest for more research into this issue.  What Is PCS-Related Brain Fog? Why Does It Matter? More than 200 PCS symptoms have been identified, with neurological and psychiatric issues being common (CDC, 2024). Taquet et al. (2021) found that a third of PCS patients received a neurological or psychiatric diagnosis within six months of infection. Brain fog, a term for neurocognitive symptoms affecting the prefrontal cortex, impacts working memory, abstract reasoning, and executive functioning (Zadeh et al., 2023).  Even mild COVID-19 cases can lead to cognitive impairments, with these deficits often appearing within the first month post-infection (Krishnan et. al., 2022). This is concerning as the prefrontal cortex’s functions are vital to daily life. PCS-related brain fog can severely impact professional, academic, and personal relationships. One in four adults with PCS experience significant limitations to their daily activities (CDC, 2024), making it crucial to understand its potential causes– neuroinflammation, vascular dysfunction, and reduced neuronal firing– so effective treatments can be developed.  Neuroinflammation When COVID-19 infects a host, it gains access to the host’s cells by binding a Spike protein to their angiotensin converting enzyme 2 (ACE2) receptors (Shabani et al., 2023). Due to ACE2 receptors being located throughout the body, the virus quickly gains access to various types of cells, including those in the central nervous system (CNS). Normally, this enzyme is supposed to help regulate blood pressure and protect the brain by transforming angiotensin I to angiotensin II, which leads to the stimulation of the angiotensin II type 1 receptor (AT1R) (Shabani et al., 2023). However, when AT1R is activated, it can promote inflammation and neurodegeneration, leaving the CNS extremely susceptible to an invasion of COVID-19 (Shabani et al., 2023).  As this occurs, microglia– cells that eliminate any potential threats to the CNS– release pro-inflammatory cytokines which contribute heavily to the body’s immune response (Colonna & Butovsky, 2017). As the microglia continue to overcompensate with more and more cytokines, the cells can experience mitochondrial dysfunction, oxidative stress, and ultimately, a severe neuroinflammatory response called a “cytokine storm”, increasing the risk of more inflammation developing in the brain (Gorenshtein et al., 2024).  Vascular Dysfunction and the Blood-Brain Barrier Cytokines can also compromise the blood-brain barrier (BBB), a selective membrane that lines the brain’s blood vessels and protects the brain by preventing harmful substances from entering. The BBB is composed of tight junction proteins that hold together vascular endothelial cells, ensuring the barrier’s integrity (Shabani et al., 2023). However, Shabani et al. (2023) found the release of pro-inflammatory cytokines like IL-1, IL-6, and TNF-ɑ can degrade these proteins, making the BBB more permeable. This increased permeability allows more cytokines and the virus itself to enter the brain (Shabani et al., 2023). Additionally, cytokines stimulate Vascular Endothelial Growth Factor (VEGF) in astrocytes, which further disrupts tight junctions and exacerbates inflammation, contributing to brain fog in PCS patients (Shabani et al., 2023). Because of the weakened BBB, it can no longer effectively protect the brain and may lead to long-term neurological issues, even after the infection clears (Shabani et al., 2023). Shabani et al.'s research also mentions how elevated levels of pro-inflammatory chemokines, molecules previously linked to age-related cognitive decline, were found in Long COVID patients with cognitive deficits. Furthermore, it is also stated that changes in the brain’s white matter were found postmortem, which could explain the persistent cognitive impairment seen in those with PCS (Shabani et al., 2023). Reduced Neuronal Firing  Neuroinflammation from COVID-19 affects neurons firing in the brain, particularly in the prefrontal cortex, which is highly vulnerable to inflammation due to its reliance on calcium-dependent feedback loops (Zadeh et al., 2023). Proper neuronal function requires balanced calcium levels; too much calcium causes nearby potassium channels to open, reducing neuronal firing. They further discuss how inflammation increases calcium release within neurons through the use of cytokines, leading to reduced firing and loss of dendritic spines necessary for synaptic connections and cognitive function.  Additionally, COVID-19 increases kynurenine levels in the brain, which can be converted into either the harmful kynurenic acid (KYNA) or the protective quinolinic acid. KYNA blocks receptors (NMDAR and nic-ɑ7R) pivotal for neuron protection, contributing to cognitive issues like memory loss (Zadeh et al., 2023). Their study suggests the virus also raises GCPII levels, disrupting normal brain signaling by reducing the effectiveness of the neurotransmitter NAAG– the combined increase of KYNA and GCPII leads to more frequent potassium channel openings, further impairing neuronal firing and perpetuating cognitive dysfunction. Conclusion The cognitive impairments associated with post-COVID syndrome, specifically PCS-related brain fog, highlight the complex interplay between neuroinflammation, vascular dysfunction, and reduced neuronal firing. COVID-19’s ability to invade the CNS, disrupt the BBB, and alter neuronal signaling barely scratches the surface on the virus’s far-reaching effects on brain health. The health and wellbeing of these patients can vary, but many describe feeling hopeless about how this illness has ravaged their body. For those living with PCS or caring for someone who does, it can be disheartening. My mom has had Long COVID since 2021 and watching her struggle with her memory and be unable to do the things she once loved has been incredibly difficult.  At the beginning of this article, I spoke of how I wished to spark interest and conversation on this subject out of professional courtesy. However, personally, I wanted to explore these mechanisms so that I could understand PCS’s potential etiologies and help alleviate the challenges faced by my loved ones and others affected by this condition. These findings emphasize the urgency needed to understand this chronic illness so adequate interventions can be discovered and used to improve quality of life in PCS patients. As research continues, it is imperative to address these neurocognitive challenges and mitigate the long-term impacts of COVID-19 on mental and neurological health.  References Centers for Disease Control Prevention: COVID-19. (2024, July 12). CDC Science and the Public Health approach to long COVID . https://www.cdc.gov/covid/php/long-covid/index.html   Colonna, M., & Butovsky, O. (2017). Microglia function in the central nervous system during health and neurodegeneration. Annual Review of Immunology , 35 (1), 441–468. https://doi.org/10.1146/annurev-immunol-051116-052358   Gorenshtein, A., Liba, T., Leibovitch, L., Stern, S., & Stern, Y. (2024). Intervention modalities for brain fog caused by long-COVID: systematic review of the literature. Neurological Sciences . https://doi.org/10.1007/s10072-024-07566-w   Krishnan, K., Lin, Y., Prewitt, K. M., & Potter, D. A. (2022). Multidisciplinary Approach to Brain fog and related Persisting Symptoms Post COVID-19. Journal of Health Service Psychology , 48 (1), 31–38. https://doi.org/10.1007/s42843-022-00056-7   Shabani, Z., Liu, J., & Su, H. (2023). Vascular dysfunctions contribute to the Long-Term cognitive deficits following COVID-19. Biology , 12 (8), 1106. https://doi.org/10.3390/biology12081106   Taquet, M., Geddes, J. R., Husain, M., Luciano, S., & Harrison, P. J. (2021). 6-month neurological and psychiatric outcomes in 236 379 survivors of COVID-19: a retrospective cohort study using electronic health records. The Lancet Psychiatry , 8 (5), 416–427. https://doi.org/10.1016/s2215-0366(21)00084-5   World Health Organization: WHO. (2022, December 7). Post COVID-19 condition (Long COVID) . https://www.who.int/europe/news-room/fact-sheets/item/post-covid-19-condition   Zadeh, A. F., Arnsten, A. F. T., & Wang, M. (2023). Scientific Rationale for the Treatment of Cognitive Deficits from Long COVID. Neurology International , 15 (2), 725–742. https://doi.org/10.3390/neurolint15020045

Written by: Vasiliki Maria Loukaki From predator to prey, carnivore to herbivore, vertebrate to invertebrate, the lives of animals appear rather distinct from one another. Yet, upon closer inspection, a series of common denominators is revealed, like a long piece of thread tying them all together. Navigation is inarguably one of these denominators, underlying their ability to forage, hunt, migrate, nest, breed, colonise, and much more. The neural underpinnings of navigation have consistently been the focus of neuroscience research ever since the momentous discovery of place cells by O’Keefe and Dostrovsky (1971). Subsequent research has revealed how humans and other animals are able to encode a mental representation of the physical world, in order to position themselves in relation to their spatial surroundings (O’Keefe & Nadel, 1978; Taube et al., 1990; Hafting et al., 2005). However, theories vary when explaining how this mental representation – commonly referred to as a cognitive map – underlies a crucial constituent of navigation; the ability to reach a spatial goal.  In their study of Egyptian fruit bats, Sarel et al. (2017) take a significant step towards deciphering the computation of goal-directed navigation by presenting the first neural evidence that supports a vector-based approach to encoding spatial goals in mammals. Historical Context The hippocampus and adjoining brain regions have been repeatedly acknowledged as an instrumental influence on navigation skills. This is primarily supported by evidence for the existence of place cells, grid cells, head-direction cells, and others that enable the construction of a cognitive map that has been speculated to underlie one’s navigation through the physical world (Moser et al., 2008; Spiers & Barry, 2015; Behrens et al., 2018). Although these cells are efficient at encoding the location and orientation of the individual in space, they do so irrespectively of spatial goals. This marks a crucial gap in navigation research, especially when considering that the ability to reach a spatial goal is the entire purpose of navigation in the first place. Certain computational models have attempted to utilise properties of the aforementioned cells in order to explain how they could give rise to goal-directed navigation (Burgess, 2008). For example, theories have posed that goal-directed navigation involves planning mental routes by activating a temporal sequence of place cells that connects the location of the individual to the location of their goal (Johnson & Redish, 2007). In fact, Burgess and O’Keefe (1996) proposed one of the earliest versions of this type of model (i.e., Simple Model of Navigation). Nevertheless, no clear neural evidence has been put forward to substantiate such models. Other computational models have postulated the existence of a vectorial representation of spatial goals. Geometrically, a vector is represented as a line segment with a specific direction and length. Therefore, a vectorial representation of spatial goals would suggest the existence of neurons that encode the direction and distance of the individual in relation to the goal. Once again, Burgess and O’Keefe (1996) proposed one of the earliest versions of this type of model (i.e., Population Vector Model of Navigation). However, apart from behavioural studies that have proposed vector-based navigation as the mechanism underlying path integration in different animals, including ants (Müller & Wehner, 1988), hamsters (Etienne et al., 1998), and humans (Foo et al., 2005), no clear neural evidence has been put forward to substantiate such models. This was until Sarel et al. (2017) published their paper on Egyptian fruit bats, presenting the first neural evidence of hippocampal goal-vector cells (GVCs) that could constitute the building blocks of the vectorial representation of spatial goals that had been theoretically contemplated for over two decades. Experimental Design Sarel et al. (2017) recorded the activity of 309 hippocampal neurons from the CA1 subfield of three Egyptian fruit bats. These model animals have been widely used in navigation research, particularly due to their heads being sufficiently large to carry the wireless electrophysiology device that uses implanted electrodes to collect single-neuron recordings, while simultaneously allowing the test subjects to fly around unrestrained. Notably, these researchers have worked with Egyptian fruit bats before, having been able to discover place cells, grid cells and head-direction cells within their hippocampal formation (Rubin et al., 2014; Finkelstein et al., 2015; Geva-Sagiv et al., 2015). According to this particular experimental setup, the test subjects were able to fly around a room with a singular, standalone platform. This platform was stocked with food, conditioning the test subjects to compute it as their spatial goal.  Principal Results Sarel et al. (2017) discovered hippocampal neurons that exhibited goal-direction tuning and goal-distance tuning. More specifically, they discovered that 19% of the cells they recorded from were goal-direction cells (i.e., selectively increasing their activity whenever the bat was facing at a specific angle  away from the spatial goal) and 16% of the cells were goal-distance cells (i.e., selectively increasing their activity whenever the bat was located at a specific distance away from the spatial goal). Additionally, they discovered that a significant portion of those cells exhibited both goal-direction tuning and goal-distance tuning. These are GVCs and they selectively increase their activity both in response to when the individual is located at a specific angle  away from the spatial goal and a specific distance  away from the spatial goal. The researchers interpreted this finding as neural evidence in support of the vectorial representation of spatial goals. The fact that singular neurons are able to encode the characteristics of a vector in relation to a spatial goal entails that a population of said neurons would theoretically be able to combine their input and allow the individual to compute a continuously updated representation of its location and orientation in relation to the goal. Thus, making it possible for the individual to decode its progress by gradually minimising the angle and  distance  between itself and the goal, before ultimately reaching said goal. Historical Contribution Although GVCs have not since been discovered in other model animals (Whittington et al., 2022) they have significantly contributed to an upsurge in the discovery of vector-based models of navigation. An example of this is the discovery of object-vector cells in the entorhinal cortex of mice that seem to function similarly to GVCs with the exception of being tuned to salient objects rather than specific goals (Høydal et al., 2019). Moreover, GVCs have instigated the development of computational models that combine the two aforementioned theoretical approaches, illustrating the idea that vectorial computations are being used in tandem with place cell (Ormond & O’Keefe, 2022) and grid cell (Banino et al., 2018) activation to mediate goal-directed navigation. Conclusion Overall, the discovery of GVCs has undoubtedly broadened our understanding of goal-directed, vector-based navigation. Given that these aspects of navigation are somewhat underrepresented in academic literature – yet underlie the very functionality of navigation skills – the contributions of Sarel et al. (2017) are a landmark of advancement in the field. That being said, the fact that equivalent cells have not been discovered in other animal models is rather disappointing. Although, recent findings have revealed the existence of cells with similar coding properties in humans (Kunz et al., 2021). Further research should attempt to identify similar cells in different model animals to establish their interspecies validity as practical mediators of navigation.  A modern reconceptualisation of spatial coding has suggested that the same cells used to construct a mental representation of physical space to underlie navigation (e.g., place cells, grid cells etc.) are also being used to construct a mental representation of an “abstract” space to underlie conceptual skills (Behrens et al., 2018; Whittington et al., 2022). Perhaps, just like GVCs are being used to compute one’s approach of a spatial goal in physical space, they may also be useful for computing one’s approach of a social goal in “abstract” space – where the measures of direction and distance are more figurative. References: Banino, A., Barry, C., Uria, B., Blundell, C., Lillicrap, T., Mirowski, P., Pritzel, A., Chadwick, M. J., Degris, T., Modayil, J., Wayne, G., Soyer, H., Viola, F., Zhang, B., Goroshin, R., Rabinowitz, N., Pascanu, R., Beattie, C., Petersen, S., & Sadik, A. (2018). Vector-based navigation using grid-like representations in artificial agents. Nature , 557 (7705), 429–433. https://doi.org/10.1038/s41586-018-0102-6 Behrens, T. E. J., Muller, T. H., Whittington, J. C. R., Mark, S., Baram, A. B., Stachenfeld, K. L., & Kurth-Nelson, Z. (2018). What Is a Cognitive Map? Organizing Knowledge for Flexible Behavior. Neuron , 100 (2), 490–509. https://doi.org/10.1016/j.neuron.2018.10.002 Burgess, N. (2008). Spatial Cognition and the Brain. Annals of the New York Academy of Sciences , 1124 (1), 77–97. https://doi.org/10.1196/annals.1440.002 Burgess, N., & O’Keefe, J. (1996). Neuronal computations underlying the firing of place cells and their role in navigation. Hippocampus , 6 (6), 749–762. https://doi.org/10.1002/(SICI)1098-1063(1996)6:6<749::AID-HIPO16>3.0.CO;2-0 Etienne, A. S., Maurer, R., Berlie, J., Reverdin, B., Rowe, T., Georgakopoulos, J., & Séguinot, V. (1998). Navigation through vector addition. Nature , 396 (6707), 161–164. https://doi.org/10.1038/24151 Finkelstein, A., Derdikman, D., Rubin, A., Foerster, J. N., Las, L., & Ulanovsky, N. (2014). Three-dimensional head-direction coding in the bat brain. Nature , 517 (7533), 159–164. https://doi.org/10.1038/nature14031 Foo, P., Warren, W. H., Duchon, A., & Tarr, M. J. (2005). Do Humans Integrate Routes Into a Cognitive Map? Map- Versus Landmark-Based Navigation of Novel Shortcuts. Journal of Experimental Psychology: Learning, Memory, and Cognition , 31 (2), 195–215. https://doi.org/10.1037/0278-7393.31.2.195 Geva-Sagiv, M., Las, L., Yovel, Y., & Ulanovsky, N. (2015). Spatial cognition in bats and rats: from sensory acquisition to multiscale maps and navigation. Nature Reviews Neuroscience , 16 (2), 94–108. https://doi.org/10.1038/nrn3888 Hafting, T., Fyhn, M., Molden, S., Moser, M.-B., & Moser, E. I. (2005). Microstructure of a spatial map in the entorhinal cortex. Nature , 436 (7052), 801–806. https://doi.org/10.1038/nature03721 Høydal, Ø. A., Skytøen, E. R., Andersson, S. O., Moser, M.-B., & Moser, E. I. (2019). Object-vector coding in the medial entorhinal cortex. Nature , 568 (7752), 400–404. https://doi.org/10.1038/s41586-019-1077-7 Johnson, A., & Redish, A. D. (2007). Neural Ensembles in CA3 Transiently Encode Paths Forward of the Animal at a Decision Point. Journal of Neuroscience , 27 (45), 12176–12189. https://doi.org/10.1523/jneurosci.3761-07.2007 Kunz, L., Brandt, A., Reinacher, P. C., Staresina, B. P., Reifenstein, E. T., Weidemann, C. T., Herweg, N. A., Patel, A., Tsitsiklis, M., Kempter, R., Kahana, M. J., Schulze-Bonhage, A., & Jacobs, J. (2021). A neural code for egocentric spatial maps in the human medial temporal lobe. Neuron , 109 (17), 2781-2796.e10. https://doi.org/10.1016/j.neuron.2021.06.019 Moser, E. I., Kropff, E., & Moser, M.-B. (2008). Place Cells, Grid Cells, and the Brain’s Spatial Representation System. Annual Review of Neuroscience , 31 (1), 69–89. https://doi.org/10.1146/annurev.neuro.31.061307.090723 Muller, M., & Wehner, R. (1988). Path integration in desert ants, Cataglyphis fortis. Proceedings of the National Academy of Sciences , 85 (14), 5287–5290. https://doi.org/10.1073/pnas.85.14.5287 O’Keefe, J., & Dostrovsky, J. (1971). The hippocampus as a spatial map. Preliminary evidence from unit activity in the freely-moving rat. Brain Research , 34 (1), 171–175. O’Keefe, J., & Nadel, L. (1978). The hippocampus as a cognitive map . Oxford University Press. Ormond, J., & O’Keefe, J. (2022). Hippocampal place cells have goal-oriented vector fields during navigation. Nature , 607 (7920), 741–746. https://doi.org/10.1038/s41586-022-04913-9 Rubin, A., Yartsev, M. M., & Ulanovsky, N. (2014). Encoding of Head Direction by Hippocampal Place Cells in Bats. 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By Davis Hobley Neural coupling, or brain-to-brain synchronization, has become an increasingly prominent area of research within computational neuroscience over the last couple of decades (Kinreich et al., 2017). With the emergence of neuroimaging techniques, such as functional magnetic resonance imaging (fMRI) in the 1990s, that can measure changes in oxygen consumption within millisecond intervals, studying brain-to-brain synchronization became much more feasible. Research in the field generally began with the work of Neurobiologist Uri Hasson and his team. They originally presented two individuals with the same stimuli and monitored their respective brain activation via fMRI. He remarkably found statistically significant correlations between these individuals time and time again (Hasson et al., 2004). Neural coupling can be measured in a few different ways, but in the case of fMRI, it tends to be a function of intersubject correlation (ISC) of BOLD signals that are produced by fMRI using magnetic resonance. ISC in this case is the extent to which the BOLD signals between two individuals rise or fall together and is rated as a value that’s between -1 and 1, with -1 being completely inversely (oppositely) correlated and 1 being completely positively correlated (overlapping). Statistical significance tests, such as t and p-value tests, are often run with calculations for ISC to determine whether or not the neural coupling observed is more likely to be or not to be due to chance (Lahnakoski & Chang, 2021). Both statistically significant positive and negative intersubject correlations are valuable for understanding neural coupling. In many studies, several ISC and significant values will be produced in large cohorts (pairs) of individuals and variables. By subsetting the data into more discrete categories, we can understand what is driving an ISC value’s total to be as high or low as it is. As it became increasingly clear that neural coupling could be implicated in learning — initially elucidated by Stephens et al. (2010) when showing significant neural coupling in successful communication between a storyteller and a listener — brain synchronization and development started to emerge as a topic in the field. As the topic focus began to shift to learning during development; however, there were originally logistical problems in studying this phenomenon. Primarily because fMRI requires study participants to stay still inside the chamber of the machine, which tends not to be a comfortable or even feasible experience for developing toddlers and infants. As a result, a newer neuroimaging technique, known as functional near-infrared spectroscopy (fNIRS), began being used in the field (Rahman et al., 2020). fNIRS works similarly to fMRI, but instead of producing a BOLD signal via magnetic resonance, it outputs concentrations of oxygenated and deoxygenated hemoglobin via light absorption and refraction, which together implicate brain activation. Additionally, it makes use of a flexible fabric cap and barely noticeable channels in contrast to the stationary fMRI. There still are logistical difficulties with the process; however, in many cases, finding a significant ISC with a small sample size is difficult, especially when employing p-value tests. The fabric caps themselves, though flexible, also often need to be repaired if infants pull at the material. Despite these difficulties, the field has been growing significantly. With the tools and capabilities to measure neural coupling in younger populations, around 2019, research quickly emerged surrounding brain synchronization between children and their caregivers. In a study by neuroscientist Piazza et al. (2019), it was first found that neural coupling between an infant and their caregiver is statistically significantly higher than the infant with a non-caregiving adult, specifically in the prefrontal cortex (PFC). This finding has provided evidence that caregiver interactions are especially important for the development of the prefrontal cortex, an area linked to processes such as emotional control, forming goals, and maintaining focus. This foundational study has provided the field with a basis for how to approach measuring neural coupling between caregivers and infants in any number of scenarios and measuring any number of factors. Figure 1 Note: The above figure shows the neural channels to have significantly significant (p < 0.05) coupling between infant and adult brains during play in a sample of 18 infant-adult dyads (Piazza et al., 2019). Over the past few years, studies intertwining neural coupling and development have become more and more prevalent, branching out and sampling various other disciplines. In 2021, a neuroendocrinology study by professors Sofia Carozza & Victoria Leong revealed that touch between parents and their infants may facilitate neural coupling and subsequent development. The same year, language development was shown to be associated with the extent to which neural coupling was occurring between infants and their caregivers (Piazza et al.). In 2022, it was suggested that the degree to which neural coupling occurs during dual-attention tasks could be correlated with later social learning (Pan et al.). More than anything, neural coupling has become a new method for evaluating almost anything and everything in the field of development, though we still might not completely understand what neural coupling means. The natural assumption could be that the more neural coupling occurring between infants and caregivers the better, though this isn’t necessarily always the case. For example, in cases where an infant is developing at a slower pace than standard, a caregiver might be more prone to inject themselves into an infant's vocal play, which could hinder their development, despite likely driving higher neural coupling (Long et al., 2022). Even assuming that neural coupling means someone is “in tune” with someone else might not necessarily be true. The meaning and interpretations of neural coupling will continue to be an integral exploration and an ongoing topic of the field. The field of neural coupling itself is still novel; the field of developmental neural coupling, even more so. As we begin to learn more about what exactly causes neural coupling during early development and its benefits or consequences, we will have yet another tool to study one of the most nuanced and involved aspects of the field: development. Bibliography Carozza, S., & Leong, V. (2021). The Role of Affectionate Caregiver Touch in Early Neurodevelopment and Parent–Infant Interactional Synchrony. Frontiers in Neuroscience , 14 . https://doi.org/10.3389/fnins.2020.613378   Hasson, U., Nir, Y., Levy, I., Fuhrmann, G., & Malach, R. (2004). Intersubject synchronization of cortical activity during natural vision. Science (New York, N.Y.) , 303 (5664), 1634–1640. https://doi.org/10.1126/science.1089506 Kinreich, S., Djalovski, A., Kraus, L., Louzoun, Y., & Feldman, R. (2017). Brain-to-Brain Synchrony during Naturalistic Social Interactions. Scientific Reports , 7 (1). https://doi.org/10.1038/s41598-017-17339-5 Lahnakoski, J., & Chang, L. (2021). Intersubject Correlation . Naturalistic-Data.org . https://naturalistic-data.org/content/Intersubject_Correlation.html Long, H. L., Ramsay, G., Griebel, U., Bene, E. R., Bowman, D. D., Burkhardt-Reed, M. M., & Oller, D. K. (2022). Perspectives on the origin of language: Infants vocalize most during independent vocal play but produce their most speech-like vocalizations during turn taking. PLOS ONE , 17 (12), e0279395. https://doi.org/10.1371/journal.pone.0279395 Pan, Y., Novembre, G., & Olsson, A. (2021). The Interpersonal Neuroscience of Social Learning. Perspectives on Psychological Science , 17 (3), 174569162110084. https://doi.org/10.1177/17456916211008429 Piazza, E. A., Cohen, A., Trach, J., & Lew-Williams, C. (2021). Neural synchrony predicts children’s learning of novel words. Cognition , 214(11), 104752. https://doi.org/10.1016/j.cognition.2021.104752   Piazza, E. A., Hasenfratz, L., Hasson, U., & Lew-Williams, C. (2019). Infant and Adult Brains Are Coupled to the Dynamics of Natural Communication. Psychological Science , 31 (1), 6–17. https://doi.org/10.1177/0956797619878698 Rahman, Md. A., Siddik, A. B., Ghosh, T. K., Khanam, F., & Ahmad, M. (2020). A Narrative Review on Clinical Applications of fNIRS. Journal of Digital Imaging , 33 (5), 1167–1184. https://doi.org/10.1007/s10278-020-00387-1 Stephens, G. J., Silbert, L. J., & Hasson, U. (2010). Speaker-listener neural coupling underlies successful communication. Proceedings of the National Academy of Sciences , 107 (32), 14425–14430. https://doi.org/10.1073/pnas.1008662107

Aditi Singh Although global democracies have consistently pledged themselves critical components of the fight against poverty, in many of these nations, poverty rates have stagnated. While the correlation between mental illness and those living under the poverty line is well-recognized, it is poorly understood, yielding persistent generational cycles of poverty that our governments lack the understanding to resolve. As a society, if we choose to recognize and characterize the impact of living under the poverty line on peoples’ brains and psychology, it will bring us one step closer to creating meaningful systemic change for those who need it the most. Across the world, living under the poverty line has been consistently linked to increased risk of psychological disorders like schizophrenia, bipolar disorder, and general anxiety disorder. While it is intuitively true that it is incredibly difficult for those with psychosis and hallucination-related disease to maintain consistent jobs, apply for social security benefits, and even attend university full-time, resulting in reduced income, psychologists eventually began asking the opposite question—what if poverty somehow propagatesmental illness? Studies have shown that diseases like schizophrenia often operate epigenetically (Wawrzczak-Bargieła et al., 2023). Fundamentally, some people are born with predispositions to certain mental illnesses, but those genes are only “turned on” when activated by environmental risk factors, such as trauma, in childhood and adolescence. When most people hear the words “childhood trauma”, their immediate association is abuse and neglect regardless of wealth, but poverty can also be a uniquely traumatizing experience asit increases the risk of both. Children under the poverty line are far more likely to witness violence in their communities, and as parental figures fall into substance abuse or continuously take on more shifts to keep their house together, they experience their own level of trauma. If both poverty and mental illness feed into one another, this relationship is possibly an additional contributor to the cyclical nature of poverty as well— if an individual begins in poverty and has a child who develops mental illness as a result of the trauma they experience, it’s unlikely that the child can escape their circumstances in the future, falling into the cycle of poverty themselves.  Aside from psychological implications, poverty directly changes brain structures. As the combination of high stress, reduced access to education, and often insufficient nutrition continue to impact developing children’s lives, it should be no surprise that their body directly manifests the toll. In a randomized experiment entitled Baby’s First Years , Dr. Kimberly Noble at Columbia University explored whether the correlation between poverty and reduced hippocampus size, lowered impulse control and altered brain pathways was, in fact, a causal relationship (Noble et al., 2022). She found that during early developmental “sensitive” periods, the brain is sculpted through processes such as the formation of new brain cells, synaptic pruning, and the development of new connections between cells. This development is specifically intended to prepare the child for the future, but when poverty’s epigenetic mechanisms impact everything from the hypothalamic pituitary adrenal axis to the nature of the sleep-wake cycle, necessary opportunities for development are fundamentally impeded. Environmentally, exposure to toxins also harms brain development. Low-income individuals, particularly refugees that have the hardest time finding access to government-subsidized housing, are likely to inhabit substandard locations with toxins such as  lead and mold exposure. A study published by the NIH found that between 2009 and 2016, over 27% of young resettled children in Ohio had blood lead levels above the healthy level. Comparatively, more than 75.5% of Afghani children of the same age had elevated blood lead levels (Shakya & Bhatta, 2019). At high levels of exposure to lead, the brain and central nervous system become severely impaired, resulting in coma, convulsions, permanent intellectual disabilities, behavioral disorders, and even death (World Health Organization, 2023). Considering that it largely affects the parts of the brain dealing with intelligence, reaction time, and attention, even if the damage is not immediately apparent, it can definitely still appear in the long term (Chiodo et al., 2004). This creates yet another mechanism for poverty to become cyclical. While the social safety nets of today seek to address almost exclusively immediate needs, perhaps a broader understanding of the psychological and biological reasons that cycles of poverty are difficult to break will enable policymakers to generate targeted, sustainably effective policies. Our society has failed the marginalized for far too long, but this unexpected step— towards the role of neuroscience in public policy— is part of our solution. References Chiodo, L. M., Jacobson, S. W., & Jacobson, J. L. (2004, March 16). Neurodevelopmental effects of postnatal lead exposure at very low levels . Neurotoxicology and Teratology. https://www.sciencedirect.com/science/article/abs/pii/S0892036204000212   MP;, S. S. (n.d.). Elevated blood lead levels among resettled refugee children in Ohio, 2009-2016 . American journal of public health. https://pubmed.ncbi.nlm.nih.gov/30998405/   Noble, K. G., & Troller-Renfree, S. V. (n.d.). The impact of a poverty reduction intervention on infant brain activity | proceedings of the National Academy of Sciences . Proceedings of the National Academy of Sciences of the United States of America. https://www.pnas.org/doi/10.1073/pnas.2115649119   Wawrzczak-Bargieła, A., Bilecki, W., & Maćkowiak, M. (2023, March 1). Epigenetic targets in schizophrenia development and therapy . Brain sciences. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046502/#:~:text=It%20is%20suggested%20that%20environmental,for%20schizophrenia%20development%20[60] .  World Health Organization. (n.d.). Lead poisoning . World Health Organization. https://www.who.int/news-room/fact-sheets/detail/lead-poisoning-and-health#:~:text=At%20high%20levels%20of%20exposure,intellectual%20disability%20and%20behavioural%20disorders .

Written by: Samantha E. De Alba Edited by: Damaris K. “Sometimes a certain smell will take me back to when I was young. How come I’m never able to identify where it comes from? I’d make a candle out of it if I ever found it...” (Twenty One Pilots, 2015) These lyrics by Twenty One Pilots, an American musical duo, are from their song, appropriately titled, “Stressed Out” which captures the overwhelming pressures of adulthood. They describe the effects that childhood scents can have on one's feelings and memories, highlighting how olfaction (the act of smelling) is the link between scent and recollection. Many of us can relate to wanting to capture the smell that takes us back to cherished moments, at least for a fleeting second. Be it the smell of freshly baked cookies, the sharp tang of pool chlorine, the earthy aroma of wet grass or any other smell one might have linked to a positive emotion. Even if we don’t exactly recall when that association formed, our sense of smell is amazing that way— unlocking memories we may have long since forgotten. But, the sense of smell is amazing in other ways too. Olfaction can offer insight into one’s brain health, prevent stress-induced neurodegeneration, and even detect Alzheimer’s. "How," you might ask? The answer is right under your nose (literally). The Biology of Olfaction and Memory Smelling involves the transport of particles to the brain's olfactory bulb, which is in charge of processing scents. After processing, the olfactory bulb relays information to the amygdala and hippocampus, the emotion and memory processing centers of the mind. (Walsh 2020). The proximity of these three regions helps explain how scents and memories become so closely intertwined. It is why certain smells transport us to moments we may have left long in the past. In fact, one’s sense of smell is one of the first senses to form, beginning in the first trimester of human development. Scent was the primary sense that guided us as infants exploring the world we were birthed into. With such heavy reliance, it is no wonder even the oldest of memories can be evoked by their scent (Nick, 2023). But like memory, the sense of smell is an ability that fades with age. While less discussed, the loss of one's sense of smell coincides with that of memory loss, occurring at around 60 years of age (Dr. Takahashi 2023; Dr. Webber, as cited in Lang 2022). Making Connections Apart from being fascinating, this connection between smell and mind can also be life-saving. Recent research found that loss of smell may indicate an increased risk of Alzheimer's disease (Velayudhan et al., 2013b). A study by Velayudhan et al. compared the olfactory impairment of participants with and without Alzheimer's (AD). It concluded that participants with Alzheimer's had notably impaired olfaction compared to the control group and that within the participants with AD, the greater the progression of the disease the weaker their ability to smell.  While we are often mindful to report changes to our memory over time, it is just as vital to pay attention to shifts in our sense of smell. Studies like the one above support the idea that olfactory and cognitive functions can be used together to assess the severity of Alzheimer's disease. But, you may wonder: if memory can be maintained and strengthened over time, how can I help preserve my sense of smell? The old saying, “stop and smell the roses,” may be more than just a reminder to be present— it's also a way to mindfully exercise and strengthen our sense of smell. Stress and Smell However, Alzheimer's is not the only way one's sense of smell can be prematurely affected. Chronic (prolonged and excessive) stress has also been shown to affect one’s smelling abilities. “ Chronic stress leads to long-term deficits in odor-driven behaviors that are critical for species survival and reproduction, and to neuroplastic changes in the nucleus of the lateral olfactory tract [which transmits information about odors to other brain regions for processing]” (Masuo et al., 2021). Stress is associated with the release of cortisol to the body, which in excess can affect your cognitive abilities and mood. Common symptoms of chronic stress include poor memory, difficulty focusing, panic attacks ,  and heightened irritability, to name a few. When a person experiences stress for extended periods, the expression of brain-derived neurotrophic factors is weakened. especially in the hippocampus, leading to neurodegeneration and increased incidence of mental disorders (Kreinin et al., 2015 as cited in Masuo 2021). Our sense of smell is so potent, that it can both induce and reduce stress. For example, while stress can be induced in numerous ways, unpleasant smells and smells with correlation to negative memories can also be enough to send one’s body into a panic. Although this may be lifesaving evolutionarily speaking, it can also be incredibly disturbing to experience over long periods. Inversely, other scents can combat the effects of stress.  A romatherapy is a natural way to calm your central nervous system and mediate these effects, which dates back to around 3000 BC (Elshafie & Camele, 2017). Using personally comforting smells, like a familiar perfume, or scents shown to improve mood, such as citrus, can help to undo some of the negative effects of stress. The influence of aromatherapy is hard to deny, as it has been proven to work both behaviorally and biologically. When participants in a study were exposed to lavender and rosemary, their cortisol levels (as tested with their saliva) significantly decreased, thus confirming their protection from the effects of stress (Atsumi & Tonosaki, 2007).  Conclusion The lyrics from Twenty One Pilots illustrate the profound connection between memory and odor, showcasing how a seemingly innocuous scent can transport one into days gone by, thereby offering comfort amidst life’s stresses. Considering this, our sense of smell is truly remarkable. It can regulate our nervous system, evoke past memories, calm, and even induce stress. It also has the ability to provide insight into the health of our brains, aiding in the detection of neurodegenerative diseases such as Alzheimer's. Let this be a reminder to ‘breathe in the moment,’ listen to our noses, and practice mindful smelling. to reduce stress and strengthen our olfactory system.  Works Cited  Atsumi, T., & Tonosaki, K. (2007). Smelling lavender and rosemary increases free radical scavenging activity and decreases cortisol level in saliva. Psychiatry Research , 150 (1), 89–96. https://doi.org/10.1016/j.psychres.2005.12.012   Chronic stress art - Google Search . (n.d.). https://www.google.com/search?sca_esv=c28229139a5cd36f&sca_upv=1&q=chronic+stress+art&udm=2&fbs=AEQNm0DfIOrc-JVK7JSIXTRypzh1d0Xgc-Qx-MWluXtsBh8oLj7QEYstEkG2d1PE1OdZoCU_yeTNdHlEnDI41QN7FfSagcIt0ZkCUulGXuGq1oJBO8FMYf_0SVjg56X1pTc_jQBsCT1f7U4HFf1UDes2Uq2kUhp4FinNOZfTYtpPjvdrIRMWzbMMeCE3fVcN8g12NXCPBDAC1-ffTC_BEJsPUYXF05Kwng&sa=X&ved=2ahUKEwie5J-O7p6IAxXahIkEHYu1IIEQtKgLegQIDxAB&biw=1440&bih=813&dpr=2#vhid=i6zcYTCS4FeGCM&vssid=mosaic   Elshafie, H. S., & Camele, I. (2017). An overview of the biological effects of some Mediterranean essential oils on human health. BioMed Research International , 2017 , 1–14. https://doi.org/10.1155/2017/9268468   Kreinin, A., Lisson, S., Nesher, E., Schneider, J., Bergman, J., Farhat, K., Farah, J., Lejbkowicz, F., Yadid, G., Raskin, L., Koman, I., & Pinhasov, A. (2015). Blood BDNF level is gender specific in severe depression. PLoS ONE , 10 (5), e0127643. https://doi.org/10.1371/journal.pone.0127643   Lavender clipart - Google Search . (n.d.). https://www.google.com/search?sca_esv=e30d006cec4fe005&sca_upv=1&q=lavender+clipart&udm=2&fbs=AEQNm0Aa4sjWe7Rqy32pFwRj0UkWd8nbOJfsBGGB5IQQO6L3J03RPjGV0MznOJ6Likin94qt3M4OQ8ZFKklfdy2IDvrI-mMI0RBJOFwr9sFw6uGAcsTGB66IS1B-o40Gw1aCAObyxPfBPbZ3lGQR-9eZ08e4pbjfZj1cuSr8YXQBwBBbOH2aeQWaDMTxKJsYWyyRZ4JMTdrfx1LpFFIqTFsho7SZ5R2r_w&sa=X&ved=2ahUKEwjei9j-852IAxWoM9AFHSnsHZgQtKgLegQIExAB&biw=1440&bih=813&dpr=2#vhid=YuhqIPyGhKVx6M&vssid=mosaic   Masuo, Y., Satou, T., Takemoto, H., & Koike, K. (2021). Smell and Stress Response in the Brain: Review of the Connection between Chemistry and Neuropharmacology. Molecules , 26 (9), 2571. https://doi.org/10.3390/molecules26092571   Nick. (2023, December 19). Why Baby’s Sense of Smell is Important | Pathways.org . Pathways.org . https://pathways.org/babys-sense-of-smell/   olfaction art - Google Search . (n.d.-b). https://www.google.com/search?q=olfaction+art&sca_esv=c28229139a5cd36f&sca_upv=1&udm=2&biw=1440&bih=813&ei=t9rSZuGrKuj9ptQP--qaoQc&ved=0ahUKEwih4_WO7p6IAxXovokEHXu1JnQQ4dUDCBI&uact=5&oq=olfaction+art&gs_lp=Egxnd3Mtd2l6LXNlcnAiDW9sZmFjdGlvbiBhcnQyBxAAGIAEGBhI-ylQjgFYiiZwAngAkAEAmAGQAaABywyqAQQwLjE0uAEDyAEA-AEBmAIOoAKFDagCAMICChAAGIAEGEMYigXCAggQABiABBixA8ICBRAAGIAEwgIEEAAYA8ICDRAAGIAEGLEDGEMYigXCAgYQABgIGB7CAgYQABgFGB7CAgkQABiABBgYGAqYAwKSBwQwLjE0oAfBQQ&sclient=gws-wiz-serp#imgrc=4KYdNc3e6fjYtM&imgdii=MPc9MksukMbXLM   Velayudhan, L., Pritchard, M., Powell, J. F., Proitsi, P., & Lovestone, S. (2013). Smell identification function as a severity and progression marker in Alzheimer’s disease. International Psychogeriatrics , 25 (7), 1157–1166. https://doi.org/10.1017/s1041610213000446

by Omegan Wright What is Oxidative Stress The human body, by design, is a highly complex, highly regulated system that maintains a tremulous balance between radical plasticity and conformity to already established functions and structures. To maintain this balance the body is compartmentalized on the cellular level, which creates trillions of microenvironments where the conditions that optimize macromolecular functions are kept stabilized. When byproducts of these processes conducted in one cellular environment invade another, significant shifts in the metabolism and eventual functionality of the cell can  develop. Oxidative stress is a term used to describe the imbalance between reactive oxygen and nitrogen species and the body's ability to remove these elements or repair the damage caused by their overabundance (Koju et al., 2019). The major consequences of oxidative stress is experienced when free radicals or free radical-causing compounds are introduced from non-native sources into a cellular environment that is less protected from their effects.  In chemically based systems like the human body, reactions between molecules occur via exchanging or sharing electrons; or, more simply, an exchange of chemical energy. Molecules are composed of atoms linked together through the sharing or exchange of electrons. In stable atoms and molecules, electrons are paired together and one bond utilizes the energy of two electrons. Having all of one's electrons paired reduces the need for an atom to go looking for an electron to pair with to create a stabilizing bond. Free radicals have only one electron that isn't paired with another electron in the outer orbital of the molecule where bonding activity occurs (Wilson, Muñoz-Palma, & González-Billault, 2018). The two types of radicals commonly involved in the dysfunctions that lead to oxidative stress are Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS). Reactive Oxygen Species (ROS)  are introduced into critical cellular environments via exogenous and endogenous sources. Exogenous sources are sources from outside the body, such as: how certain foods are prepared, environmental pollutants, heavy metals, specific drugs, chemical solvents, cigarette smoke, alcohol, and radiation (Pizzino et al., 2017). When introduced into the body, these chemicals create situations where the ROS can be produced as a byproduct or introduces ROS directly into the body. Endogenous sources of ROS come from processes within the body; these include immune cell activation, inflammation, ischemia, infection, cancer, excessive exercise, mental stress, and aging (Pizzino et al., 2017). What makes ROS production in the body so dangerous is that it can occur non-enzymatically or without the help of a molecular machine, the enzyme, to bridge the energy gap between reactants and products in the reaction. Enzymes are often highly regulated by various processes in the body that cause their activation and deactivation. ROS, RNS, and free radicals provide the body a method to bridge that reactionary gap without the help of a heavily regulated mechanism. The fact that it bypasses systemic oversight by nature leaves the body prone to allow further toxic species to be produced in the area. Common ROS, RNS, and free radical precursors implicated in oxidative stress damage are hydroxyl radicals, superoxide radicals, hydrogen peroxide, and nitrous oxide. ROS in the body (pt. I): One Organelle's Trash is Another Organelle's Treasure ROS are valuable tools in the arsenal of human metabolism. ROS allow for reactions to occur that otherwise require an excessive amount of energy to conduct on a situational or semi-regular basis. The properties of ROS allow for multiple mechanisms of usage within the human system such as, second messengers in signaling cascades, use in immune response, and use in autophagy. Autophagy is the recycling of damaged/old intracellular structures for nutrient synthesis; the ROS act as regulators in the autophagy process (Petersen, 2017). Within the immune system, ROS are weaponized by the body's immune cells to destroy pathogens (Pizzino et al., 2017). ROS are critical in mitogen response or mitogen-initiated proliferation of key cells; cells used by the body to combat disease (Pizzino et al., 2017). As signaling molecules, ROS act as go-betweens for metabolic processes that trigger subsequent reactions for desired metabolic outcomes. ROS have many traits that make them good second messengers for the cell: their short life span, malleability that allows low energy interconversions of the chemical, the superoxide radicals that are already highly regulated, and they are also prolific helpers when the body needs to adapt to stressful conditions (Wilson, Muñoz-Palma, & González-Billault, 2018).  Regulation of second messenger molecules is particularly important because they are the chemicals that trigger enzymes to start and stop/delay their functioning. The balance that the body strikes is delicate and precise, with a very small margin of error for excess activity or inactivity. Unregulated messengers can cause deficiencies and harmful build-ups of the cellular products that cause dysfunctions in organelles, which eventually leads to some of the consequences of oxidative stress.  ROS in the body (pt. II): When it All Goes Wrong The regulation of ROS in the body is critical due to its use in many essential processes. These essential processes include neuronal development in the womb. Through studies of mouse gestation, it has been determined that in utero, specific ROS act as triggers for particular differentiation of neuronal stem cells that determine the number of differentiated stem cells that usually develop and will develop  in growing brains (Wilson, Muñoz-Palma, & González-Billault, 2018). It was found that having a ROS-rich environment, had long term effects on the development of specific parts of the mice's brains with hypothesized developmental impairment of neurons (Wilson, Muñoz-Palma, & González-Billault, 2018). In humans, this phenomenon is observed in individuals with Chronic Granulomatous Disease, a disease that causes a drastic change in functionality to the family of proteins utilized to sustain hippocampal neuronal hydrogen peroxide levels; children with this disease often demonstrate cognitive issues in childhood (Wilson, Muñoz-Palma, & González-Billault, 2018). Outside of gestational development, ROS can cause oxidative damage to many of the major macromolecules: lipids, proteins, and nucleic acids. Lipids have many uses in cellular makeup and metabolism, but the major function affected by free radicals is the fluidity (permeability and movement) of the lipids used to create the cell’s plasma membrane. The cell's membrane is essential in its job of maintaining the structural integrity of the cell and the filtration of components allowed to cross into and out of the cell. The fluidity of this membrane is determined by many factors, which includes the types of lipids used in its makeup, the number of proteins embedded in the cell membrane, and more. A change in fluidity could mean a change in the permeability of the cell. Peroxidation of the lipids in  the cell membrane occurs through the cross-linking of lipids with carbon double bonds. Lipids with carbon double bonds are referred to as unsaturated lipids because the double bond between two carbon atoms prevents the formation of a carbon-hydrogen bond on those carbon atoms. These double bonds involve four electrons to hold the carbon atoms together; one or two electrons can be removed without breaking the link between the carbon atoms completely. Free radicals are unstable molecules that want to find a single electron to pair with to help stabilize themselves. The breaking of one bond between the lipids' double carbon bonds then will donate a single electron to a free radical, the radicalized or oxidized lipid and the now stable free radical create an overall more stable end product than the previous formation of the molecules (Petersen, 2017). The reaction’s end product leaves the previously stable unsaturated lipid as an unstable free radical molecule ready to react with other unsaturated molecules and so on, a phenomenon known as chain-growth polymerization. The polymerization makes the membrane more rigid, making it harder to get specific molecules across the membrane (Petersen, 2017).   Proteins are also prone to free radicals, the loss of a single electron on the protein causing destabilization leading to a change in protein conformation. A change in the conformation of a protein is similar or parallel to a machine with a component warped out of place, causing the machine to malfunction; this occurs more disastrously in enzymes (Pizzino et al., 2017).  DNA is the key nucleic acid that encodes all information that’s needed for the cell to function; changes to this code can lead to changes in the product conveyed. Free radicals, ROS, and RNS all can cause damage to DNA altering the information it encodes directly and indirectly. The consequences of the damage could be a change in the conformation of a protein, leading to the aforementioned issues or changes in access to this code prohibiting the creation of certain proteins. Certain organelles are prone to becoming the sources of these endogenous reactive oxygen species within the human body. These organelles primarily handle reactions that involve free radical intermediates; when the processes that produce these intermediates exceed/surpass the mechanisms implemented by the cell to reduce ROS concentrations, oxidative stress can occur. The mitochondria is one of these organelles. As is well known by most high school sophomores, the mitochondria is the powerhouse of the cell; the process used to make the most commonly used power source of the cell (ATP) is oxidative phosphorylation. Oxidative phosphorylation is a multi-step operation that uses free radical intermediates when chemical energy is being transferred between enzymatic processing centers, and a superoxide radical is created during this process (Wilson, Muñoz-Palma, & González-Billault, 2018). ATP (adenosine triphosphate) or a derivative is required for many higher order metabolic functions making the fact that it produces such a hazardous and prolific by-product so unfortunate. Mitochondrial dysfunction can lead to oxidative stress, a consequence of which is the continuation of axon degeneration seen in many neurological diseases. The peroxisome is another organelle that commonly causes the introduction of ROS into the cellular environment. For this specific organelle, many electron transfer reactions occur. The peroxisome produces many free radicals, including H2O2, O2- OH•, and NO• (Phaniendra, Jestadi, & Periyasamy, 2015). The endoplasmic reticulum also has enzymes contributing to ROS formation (Phaniendra, Jestadi, & Periyasamy, 2015). Organelle dysfunction is a major component of endogenous ROS proliferated oxidative stress, and it has disastrous consequences for cells that function longer than others and are sensitive to changes in the extracellular environment; like neurons. ROS in the Brain   The brain and nervous system are particularly susceptible to oxidative stress, which is a factor in many disease outcomes, such as chronic and degenerative diseases, which speeds up the body's aging process, and also acute pathologies; such as trauma and strokes (Pizzino et al., 2017). Examples of specific diseases and illnesses involved with oxidative stress are: Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, depression, dementia, and memory loss (Pizzino et al., 2017).  In Alzheimer's disease, the Nrf2 pathway, which is used to repair the damage caused by ROS species to organelles and macromolecules, when it’s disrupted; it leads to the build-up of β-Amyloid plaques. This is suspected to cause neuron loss and eventual progression to dementia, which is typical for diseases like Alzheimer’s (Ashrafizadeh et al., 2020).  Parkinson's disease is the loss of dopaminergic neurons facilitated by the deposition of Lewy bodies or protein plaque deposits of 𝛼-synuclein on the neurons, disrupting the ability of the neuron to produce dopamine (Phaniendra, Jestadi, & Periyasamy, 2015). The dopaminergic neurons most affected by Parkinson's are the neurons located in the substantia nigra, an area of the midbrain that is connected to learning, memory, and motor control (Phaniendra, Jestadi, & Periyasamy, 2015). When the neurons experience oxidative damage, the damage proliferates due to the further imbalance of the pathway, which affects  the synthesis of dopamine and damages the neuron itself (Phaniendra, Jestadi, & Periyasamy, 2015). The damage to the neuron causes a dopamine deficit; the symptoms of a dopamine deficit include: jerky movements, trembling of the hands and lips, and tremors (Phaniendra, Jestadi, & Periyasamy, 2015). Multiple sclerosis is a disorder caused by demyelination of the central nervous system, which impairs the nerves’ ability to conduct signals due to the immune system attacking itself (Phaniendra, Jestadi, & Periyasamy, 2015). Nerve conduction issues are caused by the nerve's demyelination because the nerve's insulation is worn out. The overpopulation of ROS by microglia phage and macrophage cells of the immune system causes lipid peroxidation and the eventual demyelination and damage of neurons (Phaniendra, Jestadi, & Periyasamy, 2015). How the Body Repairs Oxidative Damage The body repairs and mitigates oxidative damage via the antioxidant defense system. The antioxidant defense system is a set of mechanisms the cell uses to compensate for the damage caused to the macromolecules and organelles affected by reactive oxygen species (ROS). One of the major processes used to reduce damage to macromolecules is the Nrf2 pathway; this pathway triggers the expression of antioxidant enzymes which activates the expressions of: the heme oxygenase-1 (HO-1), NADPH quinone reductase-1 (NQO1), superoxide dismutase (SOD), glutathione-s-transferase (GST) genes (Ashrafizadeh et al., 2020). The Nrf2 pathway is considered the command center of the antioxidant defense system because it plays one of the most critical roles in maintaining the balance of the cell (Ashrafizadeh et al., 2020). The molecule Hydrogen sulfide (H2S​) is primarily produced by the mitochondria. It has cytoprotective functions that mitigate the effects of protein persulfidation caused by ROS (Zhou & Wang, 2023). In neural systems, H2S has antioxidant activity; in animals, it acts as a neuroprotective factor in neurodegenerative diseases perpetuated by mitochondrial dysfunction (Zhou & Wang, 2023).  The NOX family of proteins is also a part of the antioxidant defense system. It’s a part of the defense system because it regulates the levels of hydrogen peroxide in hippocampal neurons (Wilson, Muñoz-Palma, & González-Billault, 2018). In Chronic Granulomatous Disease the NOX family of proteins are inactivated and the buildup of hydrogen peroxide in the brain damages the surrounding neurons (Wilson, Muñoz-Palma, & González-Billault, 2018).  Potential Treatments   The most commonly recommended treatment doctors prescribe for oxidative stress is antioxidants, as they are widely regarded as a way to mitigate the effects of oxidative stress. Antioxidants can complete this function because they act to neutralize free radicals by donating an electron to the molecule and stabilizing it (Lobo, Patil, Phatak, & Chandra, 2010). Antioxidants are also easy to prescribe because they exist in many common food items that contain oils and fats that protect the food against oxidation (Lobo, Patil, Phatak, & Chandra, 2010). Antioxidants are naturally produced by the body, but in some cases, supplementation is prudent for preventative or minor corrective action combating oxidative stress (Pizzino et al., 2017). A newer treatment for oxidative stress is microRNA-based therapies. MicroRNAs are nucleic acids that do not code for proteins but are hypothesized to be involved in apoptosis, cell proliferation and differentiation, the cell cycle, and the cell's survival (Ashrafizadeh et al., 2020). In therapies, the microRNA is used to modulate oxidative pathways, specifically the over-expression of miR-371-5p and other macromolecules like to suppress oxidative stress and stimulate neuronal repair in spinal cord injuries and more (Ashrafizadeh et al., 2020). MicroRNA-based therapy is a cutting-edge approach to a new and prolific problem that affects many systems and plays a role in the worst symptoms of many diseases.  Oxidative stress has a hand in many disease pathways but is not generally discussed within general circles. People are told about antioxidants but not why the antioxidants work or what they do. Understanding the complex science isn’t too far outside the reach of the average adult, and better understanding of what supplement they’re taking  or the dietary changes the physician is recommending, will only cause a more informed and dedicated patient. Further research into how widespread an impact oxidative stress has on metabolic dysfunctions and potential novel treatments need to be explored in the future. References   Ashrafizadeh, M., Ahmadi, Z., Samarghandian, S., Mohammadinejad, R., Yaribeygi, H., Sathyapalan, T., & Sahebkar, A. (2020). MicroRNA-mediated regulation of Nrf2 signaling pathway: Implications in disease therapy and protection against oxidative stress. Life sciences , 244 , 117329. https://doi.org/10.1016/j.lfs.2020.117329 Koju, N., Taleb, A., Zhou, J., Lv, G., Yang, J., Cao, X., Lei, H., & Ding, Q. (2019). Pharmacological strategies to lower crosstalk between nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie , 111 , 1478–1498. https://doi.org/10.1016/j.biopha.2018.11.128 Lobo, V., Patil, A., Phatak, A., & Chandra, N. (2010). Free radicals, antioxidants and functional foods: Impact on human health. Pharmacognosy reviews , 4 (8), 118–126. https://doi.org/10.4103/0973-7847.70902 Phaniendra, A., Jestadi, D. B., & Periyasamy, L. (2015). Free radicals: properties, sources, targets, and their implication in various diseases. Indian journal of clinical biochemistry : IJCB , 30 (1), 11–26. https://doi.org/10.1007/s12291-014-0446-0 Pizzino, G., Irrera, N., Cucinotta, M., Pallio, G., Mannino, F., Arcoraci, V., Squadrito, F., Altavilla, D., & Bitto, A. (2017). Oxidative Stress: Harms and Benefits for Human Health. Oxidative medicine and cellular longevity , 2017 , 8416763. https://doi.org/10.1155/2017/8416763 Petersen R. C. (2017). Free-radicals and advanced chemistries involved in cell membrane organization influence oxygen diffusion and pathology treatment. AIMS biophysics , 4 (2), 240–283. https://doi.org/10.3934/biophy.2017.2.240 Wilson, C., Muñoz-Palma, E., & González-Billault, C. (2018). From birth to death: A role for reactive oxygen species in neuronal development. Seminars in cell & developmental biology , 80 , 43–49. https://doi.org/10.1016/j.semcdb.2017.09.012 Zhou, L., & Wang, Q. (2023). Advances of H₂S in regulating neurodegenerative diseases by preserving mitochondria function. Antioxidants, 12 (3), 652.   https://doi.org/10.3390/antiox12030652

Katherine Wilkinson Image source: https://bhsregister.com/5081/opinion/yes-i-can-sit-still-yes-i-am-a-girl-and-yes-i-have-adhd/   Countless thoughts tripping over one another always at the most inconvenient of times, too many to fit in your head but they do anyway. Gaze drifts during conversations, school, fun activities, and everywhere else, but you never realize it until it’s too late. Fidgeting takes place at the most inconvenient times because you don’t feel quite right existing in your own body. At other times, your body feels like a stubborn child, refusing to do what you want it to do even if it’s important. You hear someone say something thought-provoking, and the insatiable urge to blurt out whatever thought happens to be loudest takes over. Although off-putting to your peers, that doesn’t stop you from doing it. Emotions are not something you feel; they are something you become. It’s all day, every day. You wish you could handle it like everyone else is, but little do you know, most people don’t have to.   Attention-deficit hyperactivity disorder (ADHD) is a neurological disorder affecting children and adults that is categorized by difficulty managing attention, issues with controlling impulses, and/or overwhelming hyperactivity and causes problems in school, work, relationships, friendships, or caring for oneself. There are three subtypes: hyperactive, inattentive, and combined (American Psychiatric Association, 2022). While ADHD is one of the more well-known neurological disorders, there are still many children who fly under the radar and struggle through life without being evaluated for it. The majority of these children are female.  In recent years, an average of 12.5% of U.S. households had at least one male child with an ADHD diagnosis, while only 6.7% of U.S. households had at least one female child with an ADHD diagnosis (Centers for Disease Control and Prevention, 2019-2022). The current male-to-female diagnosis ratio is 2:1 in children and 1.6:1 in adults (American Psychiatric Association, 2022). However, in prior years, the male-to-female ADHD diagnosis ratio was estimated to be 10:1 (American Psychiatric Association, 1980). While these data may imply that there are simply more males than females with ADHD, that is likely not the case. On average, females receive their diagnoses four years later than their male counterparts despite having higher rates of psychiatric comorbid disorders (Skoglund et al., 2023). These differences are present due to a lack of inclusion of females in ADHD research, which is still present today but not to the same degree as previously. This has led to a deficiency in information about how ADHD presents in females and fueled biases in evaluation, treatment, and public perception of this disorder. Teachers and the general public have reported believing in the increased prevalence of ADHD in boys compared to girls, and teachers had a more difficult time identifying ADHD in girls than boys (Quinn & Wigal, 2004).  ` Although females are still capable of presenting the symptoms most common in males, the most common type of ADHD diagnosed in females is inattentive (Biederman et al., 1999; Gershon, 2002) which is associated with symptoms like lack of attention to detail, making careless mistakes, difficulty in organizing and planning activities, losing items frequently, and reluctance to begin tasks which require sustained mental effort. These differences in symptom presentation and overall disorder experience are influenced by social and biological factors (American Psychiatric Association, 2022). In females, inattentive symptoms are often associated with laziness and personal flaws rather than ADHD, and these perceptions have impacted the frequency of diagnosis within this population. Females are more likely to receive a diagnosis and pharmacological treatment if they display more outwardly noticeable symptoms of ADHD such as issues with conduct or hyperactivity (Mowlem et al., 2018), which are not as common in the inattentive subtype compared to hyperactive. Even when ADHD is diagnosed in childhood, these children and adolescents still struggle with creating and maintaining friendships (Blachman & Hinshaw, 2002; Young et al., 2004), self-harm (Rucklidge & Tannock, 2001), and self-esteem (Mazzone et al., 2013). Even though females tend to develop more coping strategies to mask their symptoms and attempt to fit into society, this does not mean that they are not struggling. Throughout their lifetimes, females with ADHD are at increased risk for mood disorders, substance abuse, attempting suicide, frequently utilizing emotion-based coping mechanisms, teen pregnancy, and borderline personality disorder (Beauchaine et al., 2019; Biederman et al., 2006; Chronis-Tuscano et al., 2010; Rucklidge & Kaplan, 1997; Skoglund et al., 2019).  ADHD going undiagnosed and untreated in females can have detrimental consequences. Without access to treatment and accommodations, late-diagnosed females will struggle more than their non-ADHD female counterparts in the areas previously mentioned. Because inattentive ADHD is more likely to last throughout the lifetime (Döpfner et al., 2015; Larsson et al., 2011) and is the most significant predictor of academic success as opposed to hyperactivity (Pingault et al., 2011), it is even more important that interventions are made during childhood to reduce negative impacts caused by ADHD-related struggles. Across males and females, later diagnosis is associated with increased mortality (Dalsgaard et al., 2015). Although there is limited research about the age of diagnosis and treatment and its effects on outcomes on ADHD symptom severity, receiving help in those areas, whether it is through psychotherapy, pharmacological treatment, or another form of intervention, would most certainly help improve quality of life. Receiving an ADHD diagnosis can have positive effects such as reducing self-blame and hatred for the existence of ADHD symptoms, developing a more thorough understanding of oneself, appreciating positive qualities associated with ADHD, and aiding peers in understanding how one’s thinking or behavior is associated with their ADHD (Halleröd et al., 2015; Morgan, 2023). Next, having an official diagnosis provides access to treatments of many forms. For example, prescribed stimulant medication can alleviate symptoms soon after taking it, unlike other non-stimulant depression and anxiety medications, which can take weeks to take effect. Different forms of treatment like ADHD coaching, cognitive-behavioral therapy, meta-cognitive therapy, and neurofeedback training have been shown to positively affect and improve symptom management in children and adults with ADHD (Arns et al., 2009; Kubik, 2010; Miranda & Presentación, 2000; Moreno-García et al., 2019; Solanto et al., 2010; Young et al., 2020). The absence of ADHD treatment can contribute to worse outcomes compared to those without ADHD, and the majority of those with ADHD who received treatment significantly benefited from it when compared to those with untreated ADHD (Shaw et al., 2012). 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