Part 1: The Mesolimbic Pathway Written by: Desiree Lano Image credit: https://www.cedars-sinai.org/newsroom/wired-for-life-study-links-infants-brain-circuitry-to-future-health/ To the layperson, dysfunction of dopamine (DA) has long been considered a major contributor to the pathophysiology of schizophrenia (SCZ). The reality, however, is far more complicated. Enter: glutamate (Glu). As the brain’s main excitatory neurotransmitter, Glu is essential for numerous functions in the brain, including but not limited to learning; memory; and neuroplasticity (Dwyer 2024). In fact, over 80% of our synapses are classified as glutamatergic. While Glu is vital for normal brain function, excessive glutamatergic activity can ultimately lead to excitotoxicity (damage to the nervous system due to excessive activity), which is implicated in various psychiatric and neurodegenerative diseases (Lee 2024). Unsurprisingly, Glu dysfunction has been found to be just as implicated as DA when it comes to the development and progression of SCZ. This article will give a short, easy-to-digest review of what is currently known about the relationship between Glu and DA in the pathology of SCZ and how this can inform current and future treatment. (P.S.: if you’re unfamiliar with the symptoms of SCZ, feel free to refer to my former article here  for a primer.) To understand Glu’s contributions to SCZ, we need to start at one of its primary targets: the N-methyl-D-aspartate receptor, or NMDAR. The NMDAR is not necessarily the sole impetus for neurotransmitters going haywire (that is a whole other, even more complicated, topic), but it is certainly the easiest place to start. The core function of NMDARs in the brain is to receive a single message from Glu: “Go!” Now, whether that signal ultimately leads to the neuron firing depends on the cumulative input of all the other receptors involved and their  signals. Still, this is an important concept to keep in mind when we discuss how the glutamate system is involved in SCZ. Here’s a quick snapshot of what’s happening in the circuit: pyramidal glutamatergic neurons initiate the pathway in the frontal cortex. These neurons synapse onto GABA interneurons also in the frontal cortex. GABA can be thought of as Glu’s counterpart—while Glu excites, GABA inhibits. The way the brain interprets these two opposing signals is a bit like how a computer processes binary code: it’s not the individual 0s and 1s that make the message, but the combination of signals that determine a neuron’s output). This stimulation of the GABA interneuron, and the subsequent release of inhibitory GABA neurotransmitter onto the next pyramidal glutamatergic neuron, keeps the glutamatergic neuron “in check” so to say. Without this GABA interneuron keeping tabs on the glutamatergic neuron, said neuron will become overexcited and fire excessively. Given that this glutamatergic neuron projects into the midbrain VTA onto DA neurons, this overexcites the DA neurons that lead to the striatum, ultimately leading to an overabundance of DA in this area. (Buck et al. 2022) This circuit is called the “mesolimbic pathway”, one of the primary dysfunctional circuits implicated in schizophrenia. So, while DA is undeniably involved, its interaction with Glu reveals a more intricate story . So, how did this hypothetical model come to light? Believe it or not, it started with PCP and ketamine. Originally used clinically–and recreationally–as dissociative anesthetics, these drugs were observed to produce symptoms indistinguishable from positive and negative symptoms in schizophrenia. Researchers then found the mechanism of action explaining the  effects of the drug: blockade of the NMDAR (Kruse et al. 2022). The blockade in this case was thought of as an “induced” hypofunction of the NMDAR. It was hypothesized to be the cause of SCZ symptoms, and evidence supporting the hypotheses for these claims emerged soon after, with many similarities observed between chronic blockade of the NMDAR in animal models using PCP or ketamine and post-mortem brains of patients with SCZ (Kruse et al. 2022). To summarize: while excessive DA release is certainly implicated in the symptomatology of SCZ, it is not an isolated phenomenon. Glu is the troublemaker, and DA is the scapegoat. There is also the additional problem of excessive Glu leading to excitotoxicity and even more severe symptomatology as neurons die off. No wonder SCZ is so difficult to treat! While atypical antipsychotics have contributed greatly to lessening the more severe symptoms of SCZ, there is still a continued need for research aimed at  developing a more fine-tuned approach to treating the disease. This article has provided a fairly high-level overview of the interplay between Glu and DA in the pathophysiology of schizophrenia. Stay tuned for part 2 where we will explore Glu’s involvement in the mesocortical pathway–a key circuit whose dysfunction leads to the negative and cognitive symptoms of SCZ. For more detailed information, please consult the cited literature below. References Buck, S. A., Quincy Erickson-Oberg, M., Logan, R. W., & Freyberg, Z. (2022). Relevance of interactions between dopamine and glutamate neurotransmission in schizophrenia. Molecular Psychiatry , 27 (9), 3583–3591. https://doi.org/10.1038/s41380-022-01649-w   Dwyer, G. E., Johnsen, E., & Hugdahl, K. (2024). NMDAR dysfunction and the regulation of dopaminergic transmission in schizophrenia. Schizophrenia Research , 271 , 19–27. https://doi.org/10.1016/j.schres.2024.07.025   Kruse, A. O., & Bustillo, J. R. (2022). Glutamatergic dysfunction in schizophrenia. Translational Psychiatry , 12 (1). https://doi.org/10.1038/s41398-022-02253-w   Lee, H.-J., Kim, H.-Y., Oh, S. J., Son, Y., Kang, K. J., Nam, K. R., & Choi, J. Y. (2024). Administration of aripiprazole alleviates memory impairment and restores damaged glutamatergic system in 5xfad mice. Molecular Imaging and Biology , 26 (5), 879–887. https://doi.org/10.1007/s11307-024-01944-8

Ean L. Small Introduction Neurological diseases, including Parkinson’s and Alzheimer's Disease, are ever-increasing with global diagnosis expected to rise 30% by 2030 [1]. The ongoing exhaustive research efforts on central nervous system (CNS) disorders have yielded few effective treatments that cure or reverse disease progression (i.e. its pathogenesis). Despite tremendous recent progress, this failure is primarily due to the brain’s protective mechanism, the blood-brain barrier (BBB), which readily rejects beneficial drugs. In fact, the BBB limits drug uptake such that less than 0.1% of a therapeutic dose enters the brain [2]. This makes the BBB an obstacle that researchers must overcome to enhance drug delivery and ultimately cure neurodegenerative diseases. Composition of the BBB The BBB is a regulatory system that protects the brain from foreign toxins and pathogens circulating in the blood, while simultaneously allowing essential nutrients, such as iron, sugars, and other complex proteins, into the brain [3]. Without this barrier, we would be vulnerable to frequent brain infections, limiting health and longevity. The BBB is composed of four main components, which are described below: Endothelial cells:  The core contributor to the lining of cerebral blood vessels, and are responsible for interacting with different cell types in the CNS [4]. Endothelial cells are the first line of defense against toxins in the bloodstream that are trying to enter the brain. Additionally, these cells have increased mitochondrial levels, meaning they have a greater energy bandwidth dedicated to transporting beneficial molecules across the BBB [3]. Astrocytes or astroglia: Primarily responsible for cell maintenance, interaction, and mediation of cell-to-cell communication [3]. Astrocytes play a crucial role in maintaining the seamless entry of key nutrients into the brain. Interestingly, in some invertebrate species that lack all the components of our BBB, astrocytes are the primary gatekeepers between toxins and the CNS [3].  Pericytes: Essential for the integrity of the BBB by creating tight junctions. These junctions, also known as small pores, between cells prevent large proteins that could disrupt proper brain function from crossing into the CNS. Without pericytes, the BBB would be incredibly permeable, allowing entry to nearly all pathogens in the blood. Microglia: The medical staff for cells that compose the BBB. Microglia regulate neuronal division and provide nutritional support to neighboring cells, underscoring their crucial role in maintaining the integrity of the BBB [4]. These four cell types work in unison to defend the brain against potential intruders. While we appreciate the BBB for its role in preserving brain health, it also poses a significant challenge to the treatment of neurological diseases that reside in the brain. We will next cover the mechanisms by which key nutrients cross the BBB and how researchers can utilize these transport systems to develop novel drug therapies. Crossing the BBB There are various methods that the cells listed above, primarily endothelial cells, employ to facilitate the passage of nutrients into the brain. Among these are passive diffusion and physical channels through which molecules can pass. Passive diffusion is the process by which proteins can float through cell membranes, much like ghosts can move through closed doors [4]. However, this passive process is limited to small proteins, molecules that are typically not included in drugs [3,4]. Physical channels, on the other hand, allow for the passage of larger proteins through a process called receptor-mediated transcytosis (RMT), where receptors on the cell surface transport nutrients, such as iron, across the BBB (Figure 1) [4]. Transcytosis can be thought of as a concierge service that shuttles nutrients through the body's barriers, making screening unnecessary. Furthermore, the channels involved in RMT are distinct proteins that may be expressed solely on brain endothelial cells, making them an enticing target for therapeutics.  Figure 1. Receptor-mediated transcytosis (RMT) is the process by which receptors expressed on brain endothelial cells transport large proteins from the blood lumen across the BBB and into the brain parenchyma. Current and novel therapeutic strategies to circumvent the BBB Previous attempts to bypass the BBB involve highly invasive drug administration. Among the most popular include intrathecal injections, where medical practitioners administer drugs at the base of the spinal cord, injecting into the cerebrospinal fluid with the hopes that the drugs make their way into the brain via the brain stem [5]. Other invasive methods used to treat neurological diseases include convection-enhanced drug delivery (injection directly into the brain), intracranial implantation, and deep-brain stimulation [4]. As such, researchers have been impatient to develop new methods of delivering drugs to the brain safely and effectively.  Recently, scientists have engineered protein shuttles that exploit RMT to transport drugs across the BBB. These proteins, often in the form of antibodies or enzymes, target receptors on brain endothelial cells, induce the internalization of those receptors, and dissociate once inside the brain to bind their specific target (Figure 1). For instance, Denali Therapeutics currently has multiple enzyme and antibody shuttle molecules in clinical trials that utilize RMT to enhance drug delivery in the brain. These drugs are used to treat Hunter Syndrome, Frontotemporal Dementia-granulin, and Hurler Syndrome [7,8,9]. Conclusions Neurological diseases are notoriously difficult to treat, and in the case of degenerative CNS disorders, there are no current medications that cure or reverse pathogenesis. This poses a great challenge for the 3.4 billion people worldwide who are suffering from Alzheimer’s, Parkinson’s, and Multiple Sclerosis, to name a few [9]. The use of novel shuttle molecules represents a significant advancement in research aimed at crossing the BBB. Furthermore, these engineered drugs could resolve symptoms and disease progression for over 40% of the global population [9]. This research not only contributes directly to the development of drugs for CNS diseases, but it also highlights the significance of harnessing natural processes in the human body for therapeutic purposes. This article serves as a reminder that every research effort, whether large or small, plays a pivotal role in answering the underlying biological question. In the future, it will be exciting to see these shuttle drugs advance in the clinic and observe the continual progress of research in this field.  Literature Cited [1] Chen, R.C. et al. Prevalence, incidence, and mortality of PD. Neurology. https://doi.org/10.1212/WNL.57.9.1679 [2] Bajracharya R. et al. Current and Emerging Strategies for Enhancing Antibody Delivery to the Brain. Pharmaceutics.   https://doi:10.3390/pharmaceutics13122014 [3] Wu, D., Chen, Q., Chen, X. et al. The blood–brain barrier: Structure, regulation and drug delivery. Sig Transduct Target Ther . https://doi.org/10.1038/s41392-023-01481-w [4] https://www.bblsa.com/analyst-reports/2024/11/12/frontiers-in-cns-therapeutic-development- breaching-the-blood-brain-barrier [5] Fowler, M.J. Intrathecal drug delivery in the era of nanomedicine. Advanced Drug Delivery Reviews. https://doi.org/10.1016/j.addr.2020.02.006 [6] Arguello A, Meisner R, Thomsen ER, et al. Iduronate-2-sulfatase transport vehicle rescues behavioral and skeletal phenotypes in a mouse model of Hunter syndrome. JCI Insight . https://doi:10.1172/jci.insight.145445 [7] https://www.alzforum.org/therapeutics/dnl593 [8] https://www.globenewswire.com/news-release/2025/01/13/3008476/0/en/Denali-Therapeutics- Announces-Key-Anticipated-2025-Milestones-and-Priorities-to-Further-Advance-Its-Therapeutics-Portfolio-for-Neurodegeneration-and-Lysosomal-Storage-Diseases.html [9] Steinmetz, J.D. et al. Global, regional, and national burden of disorders affecting the nervous system, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021. The Lancet Neurology . https://doi.org/10.1016/S1474-4422(24)00038-3

Written by: Alondra Alamillo What does it mean to be competent to stand trial? In the U.S., competency to stand trial (CTS) is a fair requirement that all individuals going through the criminal justice system must meet in order to be deemed capable of navigating criminal proceedings and participating in their defense. However this was not always the case, as it was until the 1960 Dusky v. United States Supreme Court ruling that the right to a competency evaluation was finally asserted. Although it varies by jurisdiction, this precedent led to a generally agreed upon definition of competency across the states: that the defendant must not only understand their charges, but also be able to consult with their attorney (Roesch et al., n.d.). To accurately fulfill this requirement, both the prosecutor and the defense can submit a request to the court asking for a mental health evaluation of the defendants’ competency to be completed on behalf of the court. This evaluation referral occurs after the individual has already been arrested and thus is awaiting trial. The judge then uses the forensic evaluator’s evaluation to come to a legal determination of the next steps for the defendant. If the defendant is found to be competent, then they may proceed with criminal adjudication. However, if the defendant is found to be incompetent, then the defendant must receive competency restoration services until they’ve improved enough to be considered competent to move forward with their proceedings (Murrie et al., 2023). These restoration services for those found incompetent to stand trial (IST), though court ordered, do aim to deliver psychiatric treatment to individuals with mental illness just enough so they may proceed fairly within the criminal justice system.  How is Pleading Insanity Different? It is important to note that CTS should not be confused with a relevant but different legal term, Not Guilty by Reason of Insanity (NGRI). At times when seen in the media, these two can be misunderstood as synonyms since both evaluate the defendant’s mental state. However, CTS and NGRI differ in four significant ways: the manner in which each is introduced in court, who introduces it, who decides if it is a valid claim, and the evaluation process (RCW, 2024).  When a CTS issue is raised, it may be introduced by either the prosecutor or defense as it is crucial that the defendant is competent during their criminal proceedings to ensure fairness. On the other hand, only the defense may introduce pleas of NGRI since they are proposing that the defendant cannot be found guilty if, at the time of the crime, they were legally “insane”. Assessing if the defendant was incapable of having the intention of committing the crime, and thus is not guilty, is much more difficult to determine compared to evaluating the defendants’ present competency. This means that mental illness alone is not enough to prove NGRI, since “insanity” must negate guilt (RCW, 2024). Additionally, competency status, although evaluated by a forensic mental health evaluator, is determined by the judge in the end. When presenting an insanity plea under NGRI, the jury decides instead based on the evaluator’s opinion. Finally, compared to individuals found to be IST being placed in court-ordered restoration as a result, individuals found to be NGRI are essentially serving their sentence in a psychiatric hospital. Court-Ordered Restoration Individuals found to be incompetent to stand trial (IST) must be placed in competency restoration treatment before returning to court. As the number of people referred for a competency evaluation is increasing, not only has the demand for evaluators increased, but so has the demand for spaces that deliver treatment. The demand for evaluations and restoration can create enormous setbacks in the system and cause further harm to individuals who are IST the longer they have to wait. According to Kois et al. (2024) study, the current number of annual evaluations conducted in only 18 out of the 50 states is about 140,000 compared to 60,000 evaluations in the 2000s. Though there is a significant gap in the amount of states that collect information about their competency evaluations, this does demonstrate tremendous growth. Much of this earlier growth can be attributed to deinstitutionalization, which was the transition from mass hospitalization to more community focused care (Kois et al., 2024). When it comes to restoration treatment, it is extremely crucial that the defendant is moved as quickly as possible from a detained setting to a treatment setting. However, due to how high the demand is, this is not realistic, especially given the first come first serve basis system by which treatment is delivered after someone is deemed unfit to stand trial.  Overall, not much attention has been placed in evaluating how states are managing the competency crisis in comparison to other states. However, the study Murrie et al. 2023 conducted examining Colorado’s current attempt to deliver defendants with the most illness with more immediate help rather than those who are less acutely ill has been a recorded system. Again, due to the oversaturation and demand with impatient services, there has been a more recent push towards outpatient or even jail-based programs.  COVID’s Impact on Evaluations Video conferencing (VC) as a tool for evaluating competency is another strategy explored particularly in Colorado by looking at the role it had during COVID-19. According to Torres et al. (2021), with making the necessary switch from in-person evaluations to virtual ones, some of the biggest concerns included understanding how VC impacted defendants, especially when it came to confidentiality and privacy. As opposed to regular evaluations, defendants now possibly ran the risk of unauthorized people joining into a private Zoom room and this raised significant ethical concerns regarding the responsibility the government and mental health professionals have in ensuring confidentiality (Torres et al., 2021). Furthermore, for defendants in custody awaiting an evaluation, resources that could be used to actually conduct VC’s were very limited. Many scheduling challenges arose as limited private rooms were available for defendants to meet with their health care providers once assigned treatment as well.  With data on competence already being scarce and the gap in literature, more studies are needed to fully understand COVID’s impact on restoration and evaluations across the nation. Studies analyzing alternative treatment options other than inpatient services do acknowledge the impact that the pandemic had on the already long waitlists with reducing the capacity these treatment centers had to offer to begin with (Murrie et al., 2023). More research exploring how evaluators are currently working toward providing more outpatient treatment options in their recommendations could play a role in helping reduce these waiting times as well. More resources allocated toward restoration services are needed to help reduce the harm of this crisis. References  Clker-Free-Vector-Images. (2014, August 3). Download Hammer, Auction, Authority. Royalty-Free Vector Graphic . Pixabay. https://pixabay.com/vectors/hammer-auction-authority-attorney-311342/ Murrie, D. C., Gowensmith, W. N., Kois, L. E., & Packer, I. K. (2023). Evaluations of competence to stand trial are evolving amid a national “competency crisis.” Behavioral Sciences & the Law , 41 (5), 310–325. https://doi.org/10.1002/bsl.2620 RCW 10.77.060: Plea of not guilty due to insanity—Doubt as to competency—Evaluation—Bail—Report—Competency to stand trial status check.  (n.d.). https://app.leg.wa.gov/rcw/default.aspx?cite=10.77.060 Roesch, R., Zapf, P. A., Golding, S. L., & Skeem, J. L. (n.d.). DEFINING AND ASSESSING COMPETENCY TO STAND TRIAL . https://www.justice.gov/sites/default/files/eoir/legacy/2014/08/15/Defining_and_Assessing_Competency_to_Stand_Trial.pdf Torres, L., Gliser, C. P., Formon, D. L., Hashimoto, N., & Gray, B. T. (2021). Forensic assessment in the time of COVID-19: The Colorado experience in developing videoconferencing for evaluating adjudicative competency. Psychology, Public Policy, and Law , 27 (4), 522–536. https://doi.org/10.1037/law0000320

Hannah Speechly The origins of human language remain a central and contested question across cognitive science, linguistics, and anthropology. Although language is widely accepted as a species-specific hallmark of Homo sapiens , scholars continue to debate how it evolved. Increasing evidence suggests that language did not emerge suddenly but instead developed gradually through the interaction of domain-general cognitive capacities and socially-driven communication. At the heart of this evolutionary process lies the emergence of theory of mind - the ability to attribute mental states to others, such as their perceptions, beliefs, desires, and goals - which enabled a uniquely human kind of cooperative and flexible communication. These higher-order cognitive capacities establish a foundation for language as we know it: not just a system of signs organized through syntax, but a powerful tool for sharing intentions, negotiating meaning, and building human culture. Early theories of language evolution often emphasized a sharp divide between human language and other forms of communication. Most prominently, Noam Chomsky’s discontinuity hypothesis proposed that language emerged suddenly in humans as the result of a specific genetic mutation. This mutation then gave rise to a species- and domain-specific universal grammar : a biologically endowed mental faculty that allows children to effortlessly acquire any natural language regardless of environmental variation (Chomsky, 2010). These views placed language largely outside the bounds of broader cognitive or communicative systems, treating it as a unique computational module with little evolutionary precedent. However, this model faces substantial criticism on both evolutionary and empirical grounds. From an evolutionary perspective, it is unclear how a complex and specialized system like language could have emerged in a fully-formed state through a single mutation without clear intermediate stages (Fitch, 2010; Hurford, 2012). Additionally, empirical research shows that language development depends critically on shared attention, cooperation and rich social interaction - all of which are difficult to reconcile with a purely innate faculty (Tomasello, 2008). Contemporary cognitive science increasingly supports a continuity model, which sees language as the product of general-purpose cognitive abilities shaped by cultural transmission. For example, Ferrigno et al. (2023) found that non-human primates can process nested, recursive-like sequences, suggesting that the hierarchical structure of syntax may build on pre-linguistic pattern recognition abilities. Similarly, Futrell and Hahn (2023) argue that the architecture of language reflects domain-general constraints such as working memory limitations and processing efficiency, rather than a dedicated language module. These findings resonate with Tomasello’s (2008, 2010b) usage-based account, which frames language as emerging from cognitive capacities like sequencing, categorization, and shared intentionality. Rather than being “hardwired”, linguistic structure arises from the ways in which these abilities interact within a social context. Further support for the continuity model comes from research on iterated learning, which demonstrates how linguistic structure can emerge through repeated social transmission. In a series of experiments, Kirby et al. (2014) showed that artificial languages passed across generations of learners become more structured and learnable over time. Even without explicit instruction, learners impose regularities on input, mirroring historical linguistic changes such as the regularization of irregular English verbs (e.g., “clomb” becoming “climbed”) or the simplification of case systems, as seen in the transition from Old English (which marked nouns for gender, number, and case) to Modern English’s streamlined morphology. These findings suggest that language structure is not merely inherited, but rather shaped by cognitive biases, social interaction, and repeated learning. This evidence altogether supports a view of language evolution grounded in cognitive and social capacities that predate Homo sapiens . Rather than emerging fully formed, language likely arose through the recursive interaction of biological constraints, cultural evolution, and social cognition. Theory of Mind as a Precursor to Language A key cognitive foundation for language is theory of mind (ToM): the capacity to attribute mental states such as beliefs, desires, and intentions to others. Before the emergence of explicit mental state understanding, humans and other primates appear capable of logical inference, which plays a foundational role in behavior prediction and social reasoning. Disjunctive inference (the ability to rule out one possibility to infer another) supports goal attribution and belief tracking. Call (2004) found that chimpanzees could identify the location of hidden food by excluding empty containers, suggesting reasoning beyond associative learning. Follow-up studies ruled out alternative explanations based on perceptual cues, supporting the view that non-human apes engage in genuine inferential reasoning (Call & Tomasello, 2008). This ability also appears early in human development. 23-month-olds can perform disjunctive inference with minimal linguistic support (Mody & Carey, 2016). However, more robust and flexible reasoning emerges around age three, and is shaped by language exposure and social experience (Leahy & Carey, 2020). These results suggest that while language enriches inferential reasoning, the underlying cognitive mechanisms (such as disjunctive inference) form a key basis for theory of mind by enabling individuals to represent and evaluate others’ beliefs and intentions. ToM can be usefully divided into “mind-to-world” and “world-to-mind” orientations (Anscombe, 1957; Perner & Roessler, 2010). Mind-to-world states include beliefs, knowledge, and perceptions that aim to match external reality, while world-to-mind states include desires, goals, and intentions that motivate action toward a desired outcome. Both states are essential for language use, as effective communication depends not only on tracking these orientations, but also on domain-general reasoning like logical inference and intention attribution. These capacities enable us to interpret utterances, anticipate responses, and coordinate meaning across diverse social contexts, such as understanding a request (“Can you pass the salt?”) or a belief statement (“I thought class started at 10”). To better understand how these mentalizing abilities may have evolved, researchers have also examined these orientations in non-human primates. Evidence from great apes suggests that some ToM components have deep evolutionary roots. Chimpanzees and bonobos demonstrate awareness of others’ goals and attentional states. For instance, chimpanzees can distinguish between an experimenter who is unwilling to give them food and one who is unable due to a barrier (Call et al., 2004). They also modify their gestures based on whether their audience is visually attentive, indicating sensitivity to perception and intention (Leavens et al., 2005; Tomasello & Carpenter, 2005). These abilities fall largely within the world-to-mind domain as they involve the attribution of intentions and goals.  However, current evidence suggests that great apes struggle with the mind-to-world domain, particularly when it comes to representing beliefs that differ from reality or from their own perspective. False belief understanding is a hallmark of mature ToM that remains elusive in non-human primates. In classic false belief tasks like the “Smarties task”, a child is shown a candy box that actually contains pencils. When asked what another person would think is inside the box, children under the age of four typically answer “pencils”, revealing difficulty in decoupling their own knowledge from another’s belief (Mitchell & Lacohée, 1991). Similar tasks adapted for apes using implicit measures such as eye-tracking (as opposed to explicit, verbal measures using language) show limited evidence that they can predict behavior based on false beliefs rather than observable behavioral cues. As such, some scholars propose that apes operate with a minimal or behavior-based ToM, relying on observable cues rather than fully representing others’ mental states (Call & Tomasello, 2008). Theory of Mind in Developmental Psycholinguistics Children begin to grasp simple mental states like desires and intentions around age two, such as recognizing that someone might want something different from what they actually do (Miller, 2010). By age three, they begin to recognize that people can hold false beliefs and that these beliefs can guide behavior. By around age four, children reliably pass explicit false belief tasks (Wellman, Cross, & Watson, 2001), and even infants as young as 14 months show implicit sensitivity to others’ beliefs in controlled contexts (Onishi & Baillargeon, 2005). This growing ability to attribute beliefs and desires through both world-to-mind and mind-to-world representations enables more sophisticated social reasoning and forms the foundation for pragmatic language use, such as storytelling, persuasion, and deception. Crucially, human language allows us to explicitly refer to these mental states. We can talk about what someone thinks, wants, or knows to embed representations of others’ mental states within our utterances. This recursive thinking about others’ intentions is uniquely human and may be what allows us to go beyond merely reacting to others’ behavior. While non-human primates show some precursors to theory of mind, they do not demonstrate the same capacity for nested, symbolic representation of mental states. In contrast, human children use gaze following, joint attention, and goal attribution, emerging even in infancy, to build shared intentionality. Developmental psycholinguistics further supports this continuity between social cognition and language.  Specifically, infants segment speech by detecting statistical regularities (Saffran et al., 1996) and use cues like eye gaze to link words to referents (Baldwin, 1993). These learning mechanisms are culturally universal and emerge early, suggesting they stem from domain-general cognitive capacities rather than language-specific modules. Importantly, language acquisition unfolds gradually. Children move from single words to two-word utterances and telegraphic speech before mastering the complex syntax and pragmatics of adult speech. This developmental arc mirrors proposed evolutionary stages of language emergence, from gestural or vocal protolanguages such as “babbling” to grammatically rich symbolic systems (Jackendoff, 1999; Tomasello, 2008). Children’s systematic errors, such as overregularization (“goed,” “mouses”) or pragmatic overextension, reflect active rule-seeking behavior shaped by limited input. These learning dynamics parallel the cultural evolution of language itself, where communicative pressures and inferential processes drive structure over generations. Belief and Desire in ToM-Grounded Language This raises a key question: are belief and desire understanding, which appear to be absent from great apes given current evidence, necessary for human language? While they may not be essential for basic referential communication, they are indispensable for the kind of flexible, pragmatic, and cooperative language use that defines human interaction. As early hominins navigated increasingly complex social environments, the ability to infer others’ mental states became vital for predicting behavior, coordinating in groups, and maintaining social cohesion. This higher-order social cognition provided a framework for cooperative communication and likely conferred strong evolutionary advantages (Call & Tomasello, 2008; Tomasello, 2008). Human language is inherently cooperative. Philosopher H.P. Grice (1975) formalized this insight with his cooperative principle , which proposes that speakers and listeners tacitly adhere to shared conversational norms to ensure communication is successful. Grice’s maxims of Quantity  (say as much as needed, but no more), Quality  (say what is true), Relation  (be relevant), and Manner  (be clear and orderly), are only effective if speakers assume their interlocutors are intentional agents with shared goals. Interpreting language in light of these maxims requires understanding others’ beliefs, desires, and communicative intentions. Without this mentalistic inference, language would break down into literalism or misunderstanding (Clark, 1996; Grice, 1975). These foundational social-cognitive abilities, like shared attention, joint intentions, and goal coordination, likely evolved through the pressures of group living. Hominins who could better interpret and cooperate with others were more likely to survive and reproduce. Over time, these interactions formed the scaffolding for increasingly structured and flexible communication (Tomasello, 2014). Language, in this view, is not a standalone system but an extension of preexisting social skills honed over millions of years (Scaife & Bruner, 1975; Tomasello, 2008). The communicative function of language also points to its roots in social cognition. Scott-Phillips et al. (2015) argue that human language is fundamentally ostensive; it allows speakers to intentionally signal their communicative intentions. This emphasis on cooperative communication distinguishes humans from even our closest primate relatives. For example, chimpanzees can produce contextually appropriate vocalizations (Girrard-Butoz et al., 2022; Slocombe & Zuberbühler, 2007), but they do not demonstrate the same inferential, trust-based communication that human language relies on. The ability to coordinate attention, infer intentions, and establish shared meaning likely evolved gradually as hominin social environments became more complex. As these capacities matured, they were co-opted into increasingly elaborate communicative systems. The growing ability to attribute mental states and respond accordingly enabled humans to use language not only to exchange information, but to coordinate joint action, maintain social cohesion, and transmit cultural knowledge. These functions would have been especially adaptive in the face of environmental challenges and collective problem-solving demands, which required a high degree of cooperation and group coordination (Herrmann et al., 2007; Tomasello, 2010a). This body of evidence supports a view of language as an emergent property of the human social mind. As such, the continuity framework offers a powerful lens for understanding language acquisition, development, and the uniquely human capacity to construct and share meaning. Toward an Integrated Theory of Language Taken together, these findings support the continuity theory: language did not emerge from a sudden evolutionary leap, but through the gradual refinement of cognitive, social, and communicative capacities. From a developmental perspective, it is increasingly clear that language was scaffolded by pre-existing capacities such as joint attention, goal attribution, cultural learning, and other capacities that became more complex as early humans navigated increasingly cooperative and socially demanding environments. This perspective does not reject the biological foundations of language. On the contrary, it acknowledges that neural and anatomical adaptations, such as modifications to the vocal tract and brain regions involved in sequencing, memory, and sensorimotor integration, likely co-evolved alongside cultural pressures for more sophisticated forms of communication. Language is not a singular innovation, but rather a product of dynamic interactions between biology, cognition, and culture over evolutionary time. The continuity framework is valuable precisely because it synthesizes insights from multiple disciplines, such as linking comparative studies of primate communication with research on child development and computational modeling. It also provides a reframing of nativist observations: for instance, the fact that any typically developing child can acquire any natural language may reflect not only an innate learning capacity, but also the essential role of shared intentionality, cooperative motivation, and rich communicative environments in shaping language development. Understanding how language evolved offers more than theoretical insight. It reshapes how we think about development, cognition, and what it means to be human. Language is not simply inherited; it is recreated in every child, every conversation, and every culture. It reflects our capacity not just to speak, but to cooperate, infer, and construct shared meaning across generations. Language is not a sudden evolutionary gift but one of the most remarkable outcomes of our cumulative, social evolution. References Anscombe, G. E. M. (1957). Intention . Harvard University Press. Baldwin, D. A. (1993). Infants’ ability to consult the speaker for clues to word reference. Journal of Child Language , 20 (2), 395–418. https://doi.org/10.1017/S0305000900008345 .  Call, J. (2004). Inferences about the location of food in the great apes (Pan paniscus, Pan troglodytes, Gorilla gorilla, and Pongo pygmaeus). Journal of Comparative Psychology , 118(2), 232–241. https://doi.org/10.1037/0735-7036.118.2.232 .  Call, J., & Tomasello, M. (2008). Does the chimpanzee have a theory of mind? 30 years later. Trends in Cognitive Sciences , 12(5), 187–192. https://doi.org/10.1016/j.tics.2008.02.010 Chomsky, N. (2010). Some simple evo-devo theses: How true might they be for language? In R. K. Larson, V. Déprez, & H. Yamakido (Eds.), The Evolution of Human Language: Biolinguistic Perspectives  (pp. 45–62). Cambridge University Press. Clark, H. H. (1996). Using Language . Cambridge University Press. Ferrigno, S., et al. (2023). Recursion in the wild: evidence from a non-human primate. Nature Communications , 14, 2370. https://doi.org/10.1038/s41467-023-37816-y . Fitch, W. T. (2010). The Evolution of Language . Cambridge University Press. Futrell, R., & Hahn, M. (2023). The cognitive constraints shaping language structure. Trends in Cognitive Sciences , 27(8), 688–701. https://doi.org/10.1016/j.tics.2023.05.001 Girard-Buttoz, C., Zaccarella, E., Bortolato, T. Friederici, A. D., Wittig, R. M., Crockford, C. (2022). Chimpanzees produce diverse vocal sequences with ordered and recombinatorial properties. Communications Biology . https://doi.org/10.1038/s42003-022-03350-8 .  Grice, H. P. (1975). Logic and Conversation . In P. Cole & J. L. Morgan (Eds.), Syntax and Semantics, Vol. 3: Speech Acts (pp. 41–58). Academic Press. Herrmann, E., Call, J., Hernàndez-Lloreda, M. V., Hare, B., & Tomasello, M. (2007). Humans have evolved specialized skills of social cognition: The cultural intelligence hypothesis.  Science, 317(5843), 1360-1366. https://doi.org/10.1126/science.1146282 Hurford, J. R. (2012). The Origins of Grammar: Language in the Light of Evolution II . Oxford University Press. Jackendoff, R. (1999). Possible stages in the evolution of the language capacity. Trends in Cognitive Sciences , 3 (7), 272–279. https://doi.org/10.1016/S1364-6613(99)01333-9 .  Kirby, S., Griffiths, T. L., & Smith, K. (2014). Iterated learning and the evolution of language. Current Opinion in Neurobiology , 28, 108–114. https://doi.org/10.1016/j.conb.2014.07.014 .  Leahy, B., & Carey, S. (2020). The evolution of reasoning in young children. Child Development Perspectives , 14(2), 109–115. Leavens, D. A., Hopkins, W. D., & Bard, K. A. (2005). Understanding the point of chimpanzee pointing: Epigenesis and ecological validity. Current Directions in Psychological Science , 14(4), 185–189. Mitchell, P., & Lacohée, H. (1991). Children’s early understanding of false belief. Cognition , 39(2), 107-127. https://doi.org/10.1016/0010-0277(91)90040-B .  Mody, S., & Carey, S. (2016). The emergence of reasoning by exclusion in infancy. Cognition , 152, 150–165. Onishi, K. H., & Baillargeon, R. (2005). Do 15-month-old infants understand false beliefs? Science , 308(5719), 255–258. Perner, J., & Roessler, J. (2010). Teleology and causality in children’s theory of mind. In D. D. Hutto & M. Ratcliffe (Eds.), Folk Psychology Re-assessed  (pp. 71–90). Springer. Saffran, J. R., Aslin, R. N., & Newport, E. L. (1996). Statistical learning by 8-month-old infants. Science , 274 (5294), 1926–1928. https://doi.org/10.1126/science.274.5294.1926 .  Scaife, M., & Bruner, J. S. (1975). The capacity for joint visual attention in the infant.  Nature, 253(5499), 265–266. https://doi.org/10.1038/253265a0   Scott-Phillips, T. C., et al. (2015). Pragmatics and the origin of language. Current Biology , 25(23), R1237–R1241. Slocombe, K. E., & Zuberbühler, K. (2007). Chimpanzees modify recruitment screams as a function of audience composition. Proceedings of the National Academy of Sciences , 104(43), 17228–17233. Tomasello, M. (2008). Origins of Human Communication . MIT Press. Tomasello, M. (2010a). Why don’t apes use language?  In S. T. Parker & K. L. Gibson (Eds.), The Oxford handbook of comparative evolutionary psychology  (pp. 419-436). Oxford University Press. Tomasello, M. (2010b). Why We Cooperate . MIT Press. Tomasello, M. (2014). The ultra‐social animal. European Journal of Social Psychology, 44 (3), 187–194.   https://doi.org/10.1002/ejsp.2015 Wellman, H. M., Cross, D., & Watson, J. (2001). 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Desiree Lano Introduction Psychotomimetics, entheogens, mysticomimetics, phantasticants, hallucinogens, psychotherapeutics—however you choose to describe them, psychedelics have been down a long, winding road. Coined by early psychiatrist Humphry Osmond, the term “psychedelic” originates from the Greek word for “soul-manifesting” (psyche = soul, delos = manifest). Most psychedelics are categorized as either classical or nonclassical. Classical psychedelics, which exert their effects mainly via the 5-HT2A receptor, include lysergic acid diethylamide (LSD), 4-phosphoryloxy-N,N-dimethyltryptamine (psilocybin), N,N-dimethyltryptamine (DMT). Nonclassical psychedelics include 3,4-Methylenedioxymethamphetamine (MDMA), dexomethorphan (Robitussin, Nyquil, etc.), salvinorin A (salvia), and ibogaine (Jachimowski & Kucia 2023).  Note: While much of modern psychedelic research has focused on psilocybin and LSD, researchers have also found great benefits from other nonclassical psychedelics such as MDMA and ketamine. This article will mainly focus on psilocybin and LSD. Effects Effects vary somewhat between the various types of psychedelics, but usually have some type of effect on mood, cognition, sensation, time-space perception, and self-concept. Set and setting (i.e., one’s mindset going into the experience and the environment around them) have a great effect on the outcome of the “trip”, and the intensity of the effects are dependent on dosage (higher dose usually leads to a greater effect) (Geyer 2023). Users often report pleasurable, euphoric feelings as well as a “oneness” with their surroundings. At higher doses, a phenomenon known as “ego death” has been reported, where the user experiences a complete loss of self. In some cases, particularly with higher dosages or in patients with preexisting mental illness, psychotic symptoms can manifest (Geyer 2023). In 1998, Adolf Dittrich published the Altered States of Consciousness Rating Scale which can be used to assess the subjective state of those undergoing a psychedelic experience. The scales are as follows: oceanic boundlessness (derealization and depersonalization, ego death at higher doses), disordered thinking, delusions, or loss of control during a “bad trip”, visionary restructuration (hallucinations, altered visual and auditory perception), and loss of vigilance (drowsiness, changes in cognition). Where the participant falls on each scale is often dose dependent. (Geyer 2023) A Brief Cultural History Psychedelics have a long and storied history, having been used in many cultures past and present for rituals, divination, and curing illness. It is thought that the use of psychedelic substances to alter consciousness has dated back as far as prehistoric times (Geyer 2023). Some even believe that Ancient Greeks used ergot (a substance chemically similar LSD) to alter consciousness. Psychedelics were commonly used by shamans in sacred rituals, and to this day indigenous peoples continue to use peyote in their spiritual practices (Geyer 2023). Past, Present, and Future Past Arthur Heffter was an early pioneer of modern research of psychedelics, being one of the first to document their use in modern day by self-administering mescaline derived from peyote in 1897 to study its effects (Geyer 2023; Jachimowski & Kucia 2023).  Beringer also tried to study mental illness using mescaline in 1923, attempting to use it to mimic common symptoms of psychosis (Nichols & Walter 2020). By the early 1930’s, Erich Guttman began to investigate the therapeutic benefits of mescaline, using healthy and mentally unwell patients as subjects in his research (Nichols & Walter 2020). Soon after these initial experiments with mescaline, Albert Hoffman, a well-known figure in the world of recreational psychedelics and psychedelic research, followed suit in 1938 when he synthesized LSD for the first time, likening its effects to the symptoms of schizophrenia (Geyer 2023; Jachimowski & Kucia 2023). By 1947, LSD was being sent to researchers under the trade name “Delysid” to study its effects further. Later in 1958, Hofmann discovered the molecular structure of psilocybin, hypothesizing that its serotonin-analogous structure may be of use when studying psychosis. Psilocybin also got a rebrand, being sent to researchers along with Delysid under the name “Indocybin” (Jachimowski & Kucia 2023). Delysid and Indocybin had a relatively successful stretch of experiments, particularly after studies showed a low risk of physiological harm. It was then that researchers began using LSD, psilocybin, and mescaline to better understand and treat mental illnesses such as personality disorders, affective (mood) disorders, anxiety disorders, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), substance use disorder, and schizophrenia. It did not take long for them to realize, however, that psychotic illness can be a major contraindication for psychedelic use and is unequivocally linked to a worsening of symptoms or triggering of episodes (Jachimowski & Kucia 2023). Psychedelic research was showing promise for the treatment of mental illness throughout the 1950’s and 1960’s, with great potential already being predicted by eminent researchers. It was not long, however, before the reputation of psychedelics took a dark turn: some patients in these studies were not able to consent to the studies they participated in, and word got out about the CIA using LSD in their interrogation tactics. With an increase in recreational use, laws were swiftly enacted by the government to put a stop to psychedelic use completely, snuffing out any potential (legal) research (Geyer 2023). Present The 1990’s saw a resurgence in the scientific community’s interest in psychedelic research. Various psychedelics, both “classical” and “nonclassical” have been studied and shown evidence for its usefulness for a number of conditions, including but not limited to: Alcohol use disorder, OCD, nicotine dependence, eating disorders, chronic pain, cluster headaches, anxiety disorders, depressive disorders, and mental health problems related to terminal illness (Geyer 2023; Jachmowski 2023). Beginning in 1993 after the Heffter Research Institute was founded, the spotlight turned to psilocybin given its long use in human history and ease of administration (i.e., not needing overnight hospital stays) (Geyer 2023). 2011 saw the first randomized double-blind trial published on its effects on anxiety in cancer patients, paving the way for a new wave of studies into this phenomenon. Shortly after, in 2016, benefits were seen not only in those terminal cancer patients with anxiety, but with depressive symptoms as well. There have been a number of other studies done in the 2010’s which have found significant reduction in symptoms related to nicotine and alcohol addiction in addition to symptoms of anxiety and depression (Jachimowski & Kucia 2023). Future Though we are making headway both in the research world and general society, there is still much to be done. As of now, there is not much of a standardization for treatment and there are still legal obstacles to be surmounted. Though we lost many years to such strict regulation of potentially revolutionary treatment, hopefully one day we will get to a point where we can finally help those who have lost all hope to alleviate their mental anguish. References Geyer, M. A. (2023). A brief historical overview of psychedelic research. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging , 9 (5), 464–471. https://doi.org/10.1016/j.bpsc.2023.11.003 Nichols, D. E., & Walter, H. (2020). The history of psychedelics in psychiatry. Pharmacopsychiatry , 54 (04), 151–166. https://doi.org/10.1055/a-1310-3990   Jachimowski, A., & Kucia, K. (2023). Classical psychedelics in Psychiatry – Renaissance of interest and therapeutic perspectives. Psychiatria Polska , 57 (3), 657–670. https://doi.org/10.12740/pp/150053

Written by: Sam Tyhonas Edited by: Morgann MacDonald Introduction            As a member of Gen Z, I have noticed—both in myself and in others—a rise in anxiety and depression, along with a simultaneous decrease in attention. It isn’t just anecdotal; research backs it up. This phenomenon has been studied and has quantifiable data that helps to explain just how prevalent it is becoming, “ Gen Z individuals are facing a mental health crisis as they experience high rates of depression and anxiety...for example, one of the included studies reported that the prevalences of anxiety and depression among college freshmen were 40.3% and 45.3%, respectively...”. ( Park et al., 2024 ). In other words, nearly half of current college students are suffering from anxiety and depression. Moreover, researchers in 2022 discovered that 1 million more children were diagnosed with ADHD compared to children in 2016 (Godoy, 2024). Still, there has yet to be a study comparing the increase in mental health struggles to a decrease in attention .           It would be easy to assume that these two statistics are related, but the human mind is wired to detect patterns and connections that agree with our current bias. However, it is important to remember one of the most popular phrases within psychological sciences: ‘ correlation does not imply causation.’ When analyzing research studies, how do we know if there is a connection or not? How do we know that the sources we find are credible? In this article, I will explore the relationship between anxiety and attention, looking at whether the evidence supports a link between the two. What is Attention? Attention is crucial for learning and memory, but it is more than just the ability to concentrate for a specific amount of time. When trying to define attention from a scientific perspective, a simple way to define it would be an issue with information processing. However, Kenemans defines it more specifically as, “...the set of mechanisms that control the way we perceive stimuli, select between response alternatives, store information in or retrieve it from memory, and distribute priorities among simultaneous tasks…”  (Kenemans, 2000). In order to truly remember something, it has to be properly stored and consistently retrieved to keep the memory intact. In 1968, Richard Atkinson and Richard Shriffin created the multi-store model (as shown below), which visually expresses how memory travels through our minds. It starts with the sensory information, which can be anything that the subject is going to put into memory storage, such as a birthday, a scene from a movie, or where the remote was left last night. For the brain to register this information, it must be given attention; otherwise, it won’t be acknowledged. Once registered, it is then placed in short-term memory (STM), also called working memory. This information must be rehearsed in order to remain in STM or move to long term memory (LTM). This model shows that attention is essential—if we don’t actively focus on something, we can’t store or recall it later.  Naturally, it is impossible to constantly pay attention to everything within your surroundings and store it. However, some neurological disorders make it even harder and may prevent people from submitting important information into STM. A study by Rapport claims that “ ADHD was associated with very large impairments in working memory” (Rapport et al., 2008). Kofler further supports this claim, stating, “Overall, the current findings indicate large magnitude working memory deficits in pediatric ADHD… with population nonoverlap estimates suggesting that working memory deficits are present in approximately 75%−81% of these children” (Kofler et al., 2020). While those with ADHD endure this struggle on a daily basis, understanding attention at a molecular level may help to gain a better understanding of why these individuals lack attention. ADHD, or Attention-Deficit Hyperactivity Disorder, is one of the most well-known neurodivergent disorders that is proven to impact up to 12% of people worldwide (Biederman, J., et al). However, this percentage may be inaccurate as most ADHD studies tend to focus on  minors, even though ADHD is a life-long disorder. Some of the symptoms of ADHD include impulsivity, hyperactivity (physically or mentally), forgetfulness, and difficulty concentrating. While nearly everyone experiences these symptoms at some point, ADHD is only classified as a disorder when these symptoms interfere with daily life. This rule applies to being diagnosed with any disorder, which is why some people can experience being anxious without having an anxiety disorder. T he author of The Anxious Generation , Jonathan Haidt, also supports this claim,  “ it is healthy to be anxious and on alert when one is in a situation where there really could be dangers lurking. But when our alarm bell is on a hair trigger so that it is frequently activated by ordinary events—including many that pose no real threat—it keeps us in a perpetual state of distress. This is when ordinary, healthy, temporary anxiety turns into an anxiety disorder" (Haidt, 2024). Although Haidt is discussing anxiety in his novel, a similar mindset must be used when diagnosing any disorder; patients are often only of diagnosable criteria if their symptoms are causing a significant amount of distress to this person’s life, especially if their own symptoms begin to impact other people. It is also worth noting that ADHD-like symptoms can appear in those who do not have the disorder. For example, a teenager who is used to constant technology and social media use will become accustomed to frequent dopamine releases (which we will discuss more shortly), so they may chase after that dopamine release similarly to someone who has ADHD. Other neurodivergent disorders, such as Autism Spectrum Disorder (ASD), also share overlapping symptoms. The true difference lies in genetics and how the brain functions in comparison to neurotypical individuals. Genetics play a significant role in ADHD. One key gene linked to ADHD is the dopamine transporter gene (DAT1) , which regulates dopamine reuptake. According to researchers, “t he dopamine transporter gene ( DAT1)  was originally considered the most likely ADHD candidate gene because it is responsible for the reuptake of dopamine in the presynaptic cleft, inhibited by stimulants and also because the DAT1  knockout mouse exhibits hyperactivity and deficits in inhibitory behaviour” (Thapar et al., 2012). Although this is not the only gene to impact ADHD, it is still extremely important to mention how dopamine is involved with this disorder. Dopamine’s role in ADHD extends beyond this single gene. To provide an example of another gene known to impact ADHD, another article from the NIH states, “ People with ADHD have at least one defective gene, the DRD2 gene that makes it difficult for neurons to respond to dopamine, the neurotransmitter that is involved in feelings of pleasure and the regulation of attention” (Blum et al., 2008). Blum’s article also notes that there are at least 42 gene variants that are associated with ADHD (Blum et al., 2008), so even just those two genes don’t begin to scratch the surface of how complex neurodivergent disorders can be.  Dopamine is a critical neurotransmitter for learning and motivation. When someone is lacking in this molecule, they instinctively seek activities that provide a dopamine release. This can manifest as impulsive behaviors like excessive spending, overeating, or thrill-seeking. Although acting impulsively may be more common in ADHD patients, not all dopamine-chasing behaviors are harmful—some may channel this drive into goal-setting or hobbies. That said, even productive activities can become problematic if they interfere with self-care or essential responsibilities. Even if they do get a hit of dopamine by completing a task, it is very short-lived compared to a neurotypical brain. As a result, they continue seeking out tasks or behaviors that will provide another dopamine release, often leading to task-switching and difficulty maintaining focus. Since those with ADHD find it difficult to find a dopamine balance, many find themselves dealing with symptoms of depression. This may include lack of motivation, inability to concentrate, loss of joy in activities once found pleasurable, difficulty sleeping, increased anxiety, and more. What is Anxiety?   Although the rates of anxiety and depression among today’s youth have risen sharply during the last few decades, it is essential to establish a clear definition of what it truly means to suffer from these types of disorders, and their impact. Only then can we draw scientific conclusions about their effects on the brain’s physiology. Szuhany and Simon (2022) defined, “ Anxiety disorders are characterized by symptoms that include worry, social and performance fears, unexpected and/or triggered panic attacks, anticipatory anxiety, and avoidance behaviors” . While this definition provides a solid psychological perspective, a deeper understanding of how this connects to modern teenagers and young adults can only be established from a more neurological standpoint. A study by Blanchard et al. (2024) suggests that anxiety is more related to our primal survival instincts, specifically the expectation and preparation for a predatory attack. This primal anxiety is worsened by uncertainty, heightened vigilance, and avoidance . From both a psychological and neurobiological perspective, their definition of anxiety overlaps with behavioral avoidance. Despite the credibility of these articles, Persuinin et al. (2015) introduce another interpretation, defining anxiety as pre-encounter defense.  But what does that mean in practice, and what is considered behavioral avoidance? Blanchard et al (2024) argues that one of the requirements for anxiety is the presence of a threatening stimulus. However, in the case of disordered anxiety, the threatening stimulus may be completely fabricated or falsely anticipated. This false anticipation is likely what Persuini was describing, where pre-encounter defense refers to the body's preparatory response to a perceived, yet often nonexistent, threat. Behavioral avoidance then emerges after the subject exhibits false anticipation, usually by self-isolating to avoid harmful stimuli.            Does this growing prevalence of anxiety relate to the rapidly decreasing rates of attention within Generation Z? The only way to answer this question is to say that, in reference to the beginning of this article, correlation does not imply causation. As a scientist, I would love to say that there is a clear and concise answer to this question, and that there are ways to solve it, but scientific inquiry is rarely that simple. If this question is to be solved properly, a lot of empirical research must be performed; however, that does not mean that attention and anxiety cannot impact each other generally. For instance, there is a biopsychosocial model that scientists usually use to explain how interconnected all of the systems within our body are.          So, in this sense, attention and anxiety are connected, but their relationship is likely influenced by a variety of factors, rather than solely excessive social media use. While research has shown that social media use can contribute to increased rates of anxiety, this does not necessarily mean that the social aspect of this anxiety is directly causing a decline in attention span. There are likely multiple other explanations, but that is what makes science so exciting! There are so many possibilities, and it is okay to be wrong or to reach an inconclusive result after performing an experiment as each finding opens up so many more opportunities for discovery. I encourage continuing these discoveries to expand our current body of knowledge, which will hopefully foster a community of well-educated and generous individuals as well. What Does All This Mean?             After comparing and analyzing many different sources while writing this article, it is clear that many people, including scientists, have yet to establish a clear connection between anxiety and attention. Now that you have a better understanding of both, what can you do with your newfound knowledge? Simply put: keep researching and expanding your knowledge. Thousands of free research articles are available to the public. Getting your information from accredited sources is better than accepting the (usually incorrect) information than the AI Overview function on Google will provide. How do we know that the sources used are trustworthy? Look for a methods-section. One of the fundamental rules of scientific research is to make sure you’re reading from sources that have conducted empirical research.  This is research that is based on observed results, such as an experiment, rather than simple untested logic. A reader can often tell there is empirical research when the study includes a ‘methods'  section, which is the part of the paper that discusses the specific tools and techniques used to carry out the experiment. Yes, sometimes you might make a connection in your head that makes sense logistically, but testing and observing that connection will help confirm these theories to be true or not.  Proof-read the article.  This may sound abnormally simple, but checking for excessive spelling or grammar mistakes will give you a very easy way to determine if this study is worth your time.  Check for peer review.  This one depends on where you plan to find your articles, but try to make sure the article or study you are reading is peer-reviewed. Many databases will flag peer-reviewed articles with a certain symbol and they will often include an option to only view peer-reviewed articles. Review the references page.  These are often at the end of an article, which includes an organized list of sources the author(s) used to support their findings. Finally, trust your instincts!  Proper research takes a lot of time and dedication, so if you are reading an article and something about it seems untrustworthy, there is no harm in reading something else or doing a little more digging to determine if you should continue. Remember, while it is important to create your own original thoughts, it is equally as important to base these thoughts off of verified information. By following these five rules, determining valuable research from misinformation will become second-nature. References Blanchard, D. C., & Canteras, N. S. (2024). Uncertainty and anxiety: Evolution and neurobiology. Neuroscience and biobehavioral reviews , 162 , 105732. Blum, K., Chen, A. L., Braverman, E. R., Comings, D. E., Chen, T. J., Arcuri, V., Blum, S. H., Downs, B. W., Waite, R. L., Notaro, A., Lubar, J., Williams, L., Prihoda, T. J., Palomo, T., & Oscar-Berman, M. (2008). Attention-deficit-hyperactivity disorder and reward deficiency syndrome. Neuropsychiatric disease and treatment , 4 (5), 893–918.   https://doi.org/10.2147/ndt.s2627   Godoy, M. (2024, May 23). ADHD diagnoses are rising. 1 in 9 U.S. kids have gotten one, new study finds . NPR; NPR. https://www.npr.org/sections/shots-health-news/2024/05/23/1252941968/adhd-diagnoses-are-rising-1-in-9-u-s-kids-have-gotten-one-new-study-finds Haidt, J. (2024). The Anxious Generation: How the Great Rewiring of Childhood Is Causing an Epidemic of Mental Illness. Penguin Press.   Kenemans, J. L. (2000). Review of The psychology of attention . Journal of Psychophysiology , 14 (1), 48–50.   https://doi.org/10.1027//0269-8803.14.1.48 ) Kofler, M. J., Singh, L. J., Soto, E. F., Chan, E. S. M., Miller, C. E., Harmon, S. L., & Spiegel, J. A. (2020). Working memory and short-term memory deficits in ADHD: A bifactor modeling approach. Neuropsychology , 34 (6), 686–698.   https://doi.org/10.1037/neu0000641     Park, S. Y., Do, B., Yourell, J., Hermer, J., & Huberty, J. (2024). Digital Methods for the Spiritual and Mental Health of Generation Z: Scoping Review. Interactive journal of medical research , 13 , e48929. https://doi.org/10.2196/48929 Perusini, J. N., & Fanselow, M. S. (2015). Neurobehavioral perspectives on the distinction between fear and anxiety. Learning & memory (Cold Spring Harbor, N.Y.) , 22 (9), 417–425.   https://doi.org/10.1101/lm.039180.115   Thapar A, Cooper M, Jefferies R , et al. What causes attention deficit hyperactivity disorder? Archives of Disease in Childhood 2012; 97: 260-265   Szuhany, K. L., & Simon, N. M. (2022). Anxiety Disorders: A Review. JAMA , 328 (24), 2431–2445.   https://doi.org/10.1001/jama.2022.22744

Magdalene Dochnal The ability to perceive motion is essential in a myriad of everyday situations from knowing when it is safe to cross the street to making a cup of coffee. Part of the appeal of stop-motion films like Fantastic Mr. Fox (2009)   is that they disrupt our visual system’s preference for smooth, fluid motion. But what if your perception of motion actually resembled such stop-motion cinematography? What if you were unable to perceive motion? This condition is called akinetopsia , or motion blindness (Kumar & Wroten, 2024). It falls under a category of conditions called visual agnosias : deficits in visual perception that arise not from any abnormalities in the eye like near- or farsightedness, but in the visual areas of the brain (Kumar & Wroten, 2024). Though exceptionally rare, akinetopsia’s effects can be debilitating, and understanding how the condition arises and exploring the lived experiences of those with akinetopsia can provide great insight into how the structure of the visual system informs its function. Background The visual system can be thought of as being organized into modules that each perform specialized computations which, when synthesized, provide us with a rich picture of what our environment looks like. The middle temporal visual area ( area MT ) in the extrastriate cortex is the module responsible for processing information about motion (Born & Bradley, 2005; Dubner & Zeki, 1971). This is partially accomplished via directional selectivity: neurons selectively firing for preferred directions of motion (Hotson et al., 1994; Zeki & Dunbar, 1971). This tuning can either be broad, meaning the neuron still fires at baseline levels when a stimulus is not moving in its preferred direction, or the directional tuning can be fine, meaning activity is inhibited when a stimulus is not moving in a neuron’s preferred direction (Born & Bradley, 2005). Neurons in area MT are also tuned for the speed of a stimulus, its size, its position on the retina, and binocular disparity, the difference in a stimulus’ position on the retina of each eye (Born & Bradley, 2005; Lagae et al., 1993; Liu & Newsome, 2005). Synthesizing data from each of these properties allows us to make important judgments, such as how fast a car is moving or in what direction a ball is being thrown. Experiencing akinetopsia Akinetopsia occurs as a result of damage to or downregulation of area MT cells. The kind of neuronal damage that causes akinetopsia can occur in many ways. Across 12 reported cases, common causes included: stroke (Blanke et al., 2003; Cooper et al., 2012; Heutink et al., 2019), epilepsy (Blanke et al., 2002; Maeda et al., 2019; Sakurai et al., 2013), Alzheimer’s disease (Cárdenas-Belaunzarán & Cerrillo-Avila, 2024; Pelak & Hoyt, 2005; Tsai & Mendez, 2009), Parkinson’s disease (Sasaki et al., 2022), traumatic brain injury (TBI; Pelak & Hoyt, 2005), and drug toxicity (Horton & Trobe, 1999). Other visual agnosias like achromatopsia (cortical color-blindness) or prosopagnosia (face blindness) arise from similar damage to cells in their function’s respective visual system modules (Kumar & Wroten, 2024). The lived experiences of those with akinetopsia can vary greatly, and the factors that contribute to that variance are still largely unknown. In the most extreme cases of the condition, all objects are invisible to the viewer when they are moving, especially at high velocities or in environments with high degrees of visual noise (Blanke et al., 2002; Heutink et al., 2019; Rizzo et al., 1995; Zihl et al., 1983; Zihl & Heywood, 2015). A more common clinical presentation in case reports is cinematographic akinetopsia, where objects in motion are experienced in a series of freeze-frames or trailing images that collapse on each other as objects come to a stop (Horton & Trobe, 1999; Sakurai et al., 2013; Viscardi et al., 2024). Because area MT cells are selective for direction, some patients only experience motion blindness when an object is moving in a particular direction (Blanke et al., 2002). This presentation appears to be associated with patients whose area MT lesions are contained to only one hemisphere of the brain. For example, a patient with epileptic seizures stemming from the right amygdala and surrounding temporal and parietal areas displayed impaired motion direction discrimination for objects moving to her left along with smaller impairments to all objects moving in her left visual field (Blanke et al., 2002). Patients for whom motion direction discrimination is impaired regardless of direction typically have lesions across both hemispheres (Pelak & Hoyt, 2005; Rizzo et al., 1995; Zihl et al., 1983; Zihl & Heywood, 2015).  Some patients with akinetopsia do see their symptoms dissipate. In cases of patients with akinetopsia resulting from epilepsy, being administered the anticonvulsant carbamazepine resolved all visual symptoms (Maeda et al., 2019; Sakurai et al., 2013). For two patients who developed akinetopsia from the antidepressant nefazodone, symptoms resolved after discontinuing the drug or greatly lowering the dosage (Horton & Trobe, 1999). However, patients whose akinetopsia arises from TBI’s, strokes, or neurodegenerative disorders like Alzheimer’s and Parkinson’s are largely left with the condition for the rest of their lives (Kumar & Wroten, 2024).  Patients with more permanent area MT lesions often experience the most significant reductions in quality of life. One patient whose akinetopsia developed from a TBI was unable to engage in his favorite hobbies like hunting because his condition left him unable to distinguish fellow hunters (Pelak & Hoyt, 2005). Another patient whose akinetopsia developed from a bout with Alzheimer’s reported that they had to stop driving because they were unable to see other cars on the road or judge how fast they were driving (Pelak & Hoyt, 2005). Many patients with akinetopsia are not even aware of the full extent of their condition and thus do not end up seeing a neurologist or ophthalmologist for years. The previously mentioned patient with TBI-induced akinetopsia did not see a specialist until two years after the onset of his symptoms (Pelak & Hoyt, 2005). In extreme cases, some patients develop a pathological denial of their visual and neurological symptoms called anosognosia and may never seek treatment (Antoniello & Gottesman, 2020; Burns, 2004). Significance Treatment options for patients with akinetopsia arising from permanent brain lesions are few and far between. Therapeutic approaches to akinetopsia typically involve training patients to use perceptual cues from other sensory modalities to provide information about moving objects (Burns, 2004; Kumar & Wroten, 2024). For example, while patients often find it difficult to cross the street because they cannot see when cars are approaching, patients can use auditory information to determine whether cars are moving toward them or away from them before crossing the street. But even then, many patients with akinetopsia require consistent monitoring and close supervision to prevent injuries (Burns, 2004; Kumar & Wroten, 2024). The patients who experience the worst prognostic outcomes are those whose family or loved ones are unable to volunteer significant time to care for them or those who do not have access to at-home care.  42 years after the first reported case of akinetopsia, many questions remain incompletely answered regarding drivers of variety in clinical presentations, variance in prognostic outcomes, and case reports are still exceptionally rare. But since Zihl & colleagues’ account of Patient LM in 1983, knowledge of area MT and the field of motion perception has expanded greatly by investigating accounts of motion blindness. Research is still sorely needed to provide a more comprehensive account of this condition if more viable treatments are to be developed. References Antoniello, D., & Gottesman, R. (2020). The phenomenology of acute anosognosia for  hemiplegia. The Journal of Neuropsychiatry and Clinical Neurosciences , 32 (3), 259–265.  https://doi.org/10.1176/appi.neuropsych.19010008 Blanke, O., Landis, T., Safran, A. B., & Seeck, M. (2002). Direction‐specific motion blindness  induced by focal stimulation of human extrastriate cortex. European Journal of  Neuroscience , 15 (12), 2043–2048. https://doi.org/10.1046/j.1460-9568.2002.02038.x Blanke, O., Vaclavik, V., Landis, T., & Safran, A. B. (2003). Dog phobia in a motion-blind  patient.  Cognitive Neuropsychiatry , 8 (3), 211–221. \ https://doi.org/10.1080/13546800244000300 Born, R. T., & Bradley, D. C. (2005). Structure and function of visual area MT. Annual Review of  Neuroscience , 28 (1), 157–189. https://doi.org/10.1146/annurev.neuro.26.041002.131052 Burns, M. S. (2004). Clinical management of agnosia.  Topics in Stroke Rehabilitation , 11 (1),  1–9. https://doi.org/10.1310/N13K-YKYQ-3XX1-NFAV Cárdenas-Belaunzarán, J., & Cerrillo-Avila, K. A. (2024). Visual agnosia mimicking memory  impairment: A case report of posterior cortical atrophy.  Neuro-Ophthalmology , 48 (1),  30–36. https://doi.org/10.1080/01658107.2023.2257311 Cooper, S. A., Joshi, A. C., Seenan, P. J., Hadley, D. M., Muir, K. W., Leigh, R. J., & Metcalfe,  R. A. (2012). Akinetopsia: Acute presentation and evidence for persisting defects in  motion vision. Journal of Neurology, Neurosurgery & Psychiatry , 83 (2), 229–230.  https://doi.org/10.1136/jnnp.2010.223727 Dubner, R., & Zeki, S. M. (1971). Response properties and receptive fields of cells in an  anatomically defined region of the superior temporal sulcus in the monkey. Brain  Research , 35 (2), 528–532. https://doi.org/10.1016/0006-8993(71)90494-X Heutink, J., De Haan, G., Marsman, J.-B., Van Dijk, M., & Cordes, C. (2019). The effect of  target speed on perception of visual motion direction in a patient with akinetopsia.  Cortex , 119 , 511–518. https://doi.org/10.1016/j.cortex.2018.12.002 Horton, J. C., & Trobe, J. D. (1999). Akinetopsia from nefazodone toxicity. American Journal of  Ophthalmology , 128 (4), 530–531. https://doi.org/10.1016/S0002-9394(99)00177-4 Hotson, J., Braun, D., Herzberg, W., & Boman, D. (1994). Transcranial magnetic stimulation of extrastriate cortex degrades human motion direction discrimination. Vision Research ,  34 (16), 2115–2123. https://doi.org/10.1016/0042-6989(94)90321-2 Kumar, A., & Wroten, M. (2024). Agnosia. In StatPearls . StatPearls Publishing.  http://www.ncbi.nlm.nih.gov/books/NBK493156/ Lagae, L., Raiguel, S., & Orban, G. A. (1993). Speed and direction selectivity of macaque  middle temporal neurons. Journal of Neurophysiology , 69 (1), 19–39.  https://doi.org/10.1152/jn.1993.69.1.19 Liu, J., & Newsome, W. T. (2005). Correlation between speed perception and neural activity in  the middle temporal visual area. The Journal of Neuroscience , 25 (3), 711–722.  https://doi.org/10.1523/JNEUROSCI.4034-04.2005 Maeda, K., Sugihara, Y., & Shiraishi, T. (2019). Akinetopsia with achromatopsia due to focal epilepsy. Seizure , 67 , 27–29. https://doi.org/10.1016/j.seizure.2019.03.004 Pelak, V. S., & Hoyt, W. F. (2005). Symptoms of akinetopsia associated with traumatic brain  injury and Alzheimer’s disease. Neuro-Ophthalmology , 29 (4), 137–142.  https://doi.org/10.1080/01658100500218046 Rizzo, M., Nawrot, M., & Zihl, J. (1995). Motion and shape perception in cerebral akinetopsia.  Brain , 118 (5), 1105–1127. https://doi.org/10.1093/brain/118.5.1105 Sakurai, K., Kurita, T., Takeda, Y., Shiraishi, H., & Kusumi, I. (2013). Akinetopsia as epileptic  seizure. Epilepsy & Behavior Case Reports , 1 , 74–76.  https://doi.org/10.1016/j.ebcr.2013.04.002 Sasaki, C., Yokoi, K., Takahashi, H., Hatakeyama, T., Obara, K., Wada, C., & Hirayama, K.  (2022). Visual illusions in Parkinson’s disease: An interview survey of symptomatology.  Psychogeriatrics , 22 (1), 38–48. https://doi.org/10.1111/psyg.12771 Tsai, P.-H., & Mendez, M. F. (2009). Akinetopsia in the posterior cortical variant of Alzheimer  disease. Neurology , 73(9), 731–732. https://doi.org/10.1212/WNL.0b013e3181b59c07 Viscardi, L. H., Kleber, F. D., Custódio, H., Costa, A. B., & Brollo, J. (2024). Akinetopsia (visual  motion blindness) associated with brain metastases: A case report. Neurological Sciences ,  45 (9), 4621–4623. https://doi.org/10.1007/s10072-024-07565-x Zihl, J., & Heywood, C. A. (2015). The contribution of LM to the neuroscience of movement  vision. Frontiers in Integrative Neuroscience , 9 . https://doi.org/10.3389/fnint.2015.00006 Zihl, J., Von Cramon, D., & Mai, N. (1983). Selective disturbance of movement vision after  bilateral brain damage. Brain , 106 (2), 313–340. https://doi.org/10.1093/brain/106.2.313

By Andrew Monti Attachment Theory Humans are social animals, and it is in their nature to connect and communicate with others to form romantic and befriend relationships. Humans crave intimacy and bonding with the ones they love and enjoy being around. People display their affection and interests differently from one another in relationships, as there are four known attachment styles: secure, anxious, avoidant, and disorganized (fearful-avoidant). This all relates to the attachment theory suggested by Bowlby’s attachment theory. John Bowlby (1909-1990) was a British psychiatrist and psychoanalyst who proposed a theory that all children are born with a biological component that makes one seek and desire connection to attachment figures. Bowlby suggested that children have this objective to ensure their safety and needs are met; protecting them from any potential dangers in their environment (Cherry, 2023). Attachment Styles As briefly mentioned, there are four main attachment styles that all have distinct characteristics, all falling into two categories of secureness: secure and insecure. Secure The secure attachment style is the most ideal as it is the healthiest and most common where individuals can make relationships both intimate and friendly ( The Attachment Project,  2024). These people are in touch with their emotions and can freely express them to others. In addition, they make deep and meaningful connections to make long-lasting relationships and rely on individuals without fear. Avoidant Avoidant in one of the three insecure attachment styles as individuals with this tend to have trouble both initiating and maintaining long-lasting relationships, specifically intimate ones as their tolerance may be low for emotional and physical intimacy with people ( The Attachment Project,  2024). They can seem to be very independent as their reliance/dependence on others may be viewed as being “weak”. Anxious Anxious is another attachment style that falls in the insecure realm as these individuals fear rejection or abandonment. It is not uncommon for people with this attachment style to have low self-esteem and clinginess in relationships. They may seek frequent reassurance to calm their anxious fears of abandonment. Disorganized Disorganized, an insecure attachment style shares characteristics of the anxious and avoidant groups. People with this attachment style are inconsistent with their emotions as they fear intimacy but want relationships. Some describe these individuals as having a “push and pull” force in intimate relationships, meaning they first crave intimacy and contact but once met with it, they are overwhelmed with fear and anxiety. They may push away despite originally wanting it. How Attachment Manifests on the Brain Throughout infancy and early childhood, the brain goes under major neuroplasticity. In other words, the brain experiences dramatic development and growth. During that stage of development, attachment style can influence how the brain matures, specifically cortical thickness and subcortical volume (Puhlmann et al., 2021). Researchers (Puhlmann et al., 2021) found that self-reported individuals with both anxious and avoidant attachment styles had decreased cortical thickness; avoidant individuals showed a similar pattern in prefrontal cortical areas as well as parts of the temporal lobe. Although anxious and avoidant individuals had decreased cortical thickness, avoidants showed greater cortical thickness than anxious individuals (Puhlmann et al., 2021). Cortical thickness refers to the width of the outer brain and can be used to indicate potential signs of neurodegenerative diseases ( Cortical thickness ). So, insecure attachment individuals are more susceptible to having lower cortical thickness which is critical for the trajectory of potential future development of neurodegenerative diseases.  The amygdala is the human alarm system responsible for our flight and fight response in stressful situations. This critical function of the limbic system plays an important in attachment as it is the core of social processing and emotional learning (Admin, 2020). Since the amygdala processes external interactions, it examines every situation when acted upon; safety, danger, relationships, pleasure, and pain (Admin, 2020). And with that, any situation that has a significant impact on an individual can be stored as a long-term memory. So, early experiences in childhood can be learned and adjusted to that present throughout adult life, therefore backing up the attachment style originally forming in childhood. References Admin, H. (2020, May 26). Understanding how attachment affects the brain . Hand in Hand Family Mentorship. https://handinhandmentoring.org/understanding-how-attachment-affects-the-brain/  The Attachment Project . Attachment Project. (2024, November 25). https://www.attachmentproject.com/  Cherry, K. (2023, September 12). How John Bowlby influenced child psychology . Verywell Mind. https://www.verywellmind.com/john-bowlby-biography-1907-1990-2795514  Cortical thickness . Cortical Thickness - an overview | ScienceDirect Topics. (n.d.). https://www.sciencedirect.com/topics/computer-science/cortical-thickness  Puhlmann, L. M., Derome, M., Morosan, L., Kilicel, D., Vrtička, P., & Debbané, M. (2021). Longitudinal associations between self-reported attachment dimensions and neurostructural development from adolescence to early adulthood. Attachment & Human Development , 25 (1), 162–180.  https://doi.org/10.1080/14616734.2021.1993628

Written by: Jacinda Taggett Cognition (better known as the overall thought encompassing attention, language, decision-making, and memory) is an important aspect of daily life, yet it still has many questions unanswered. Psychologists now often lean more towards a neuroscientific approach, utilizing images and quantifications of the brain in order to answer “how” and “why” these processes happen. As psychological science starts to move towards explaining cognition through this lens, we also see an increase in wanting to study these processes in naturalistic contexts. For example, many memory studies have been done using word pairs or trivia questions to assess “long-term memory”. However, most information in which we remember is more complex than word-pair associations. Therefore, cognitive neuroscientists over recent years have started using visual media to answer scientific questions regarding human memory. Throughout this article, we will highlight a few studies in recent years that provide insights to memory, utilizing media from Oscar-nominated films to sports plays. What are our natural thought processes during media-watching? – Movie Clips Our initial study of interest incorporated three movie clips across three genres, each ten minutes long. Participants in the recent Wallace et al. (2025) study watched Citizenfour (a documentary), Little Miss Sunshine (a comedy), and 500 Days of Summer (a romance) before answering questions to test their comprehension and memory of the material. Half of these participants watched inside an fMRI scanner, to create images of the brain during this task, and the other half were at a desk, to have a more naturalistic movie-watching experience. Wallace and colleagues had found that information in these movies was more memorable if multiple senses (e.g., the visuals and audio) were highly engaging, and this effect was even more prominent with high neural activity in the parts of the brain responsible for visual and auditory processing. Likely, when events are utilizing multiple senses, and therefore leading to a more comprehensive episodic experience, they are more memorable. How does our brain separate memories into events? – NCAA Basketball When given a continuous stream of information on a daily basis, humans have adapted to segment their memories into events. In a neuroimaging study by Antony et al. (2021), the researchers aimed to answer how this event segmentation happens directly (when a person claims a new event has occurred) and indirectly (when their brain indicates a new event has occurred). Participants viewed and recalled 9 NCAA basketball plays while collecting fMRI and eye tracking data, in order to measure surprise both in brain areas and in pupil dilation. Critically, the experimenters measured surprise in the clips by calculating the change in win probability from one possession to the next. They found that surprise predicted event boundaries , both discreetly (e.g., when participants claimed a new boundary had occurred) and autonomically (e.g., the increased neural patterns of brain areas associated with vision and memory; V1, precuneus, and medial prefrontal cortex). Surprise, along with its corresponding fMRI and eye tracking measures, was associated with better long-term memory of the events. How do people remember and recall events? – Memento  (2000) Life is not always composed of linear narrative events. If someone were to describe a piece of gossip they had received from someone else, they can either describe it temporally (how they were told the story) or chronologically (how the gossip’s series of events occurred). Memento  (2000), if you have not already viewed it, implements a unique storytelling technique that directly distinguishes these two storytelling strategies. The original film is segmented into two storylines, the backwards plot-driven storyline (as seen in color; red in the figure ) and the standard plot-driven storyline (as seen in black and white; blue in the figure ). The film makes note to jump between the end of the story (in color, first scene) and the beginning of the storyline (black and white, second scene) until it meets at the direct climax at the end of the movie. Antony et al. (2024)  took this temporal versus chronological storytelling in order to answer the question “how are humans recalling events?” Participants either watched Memento  in film-production order (bouncing between timelines) or chronological order (snipped and pieced together to be one continuous storyline). They then quantitatively assessed the various ways that we can remember a film’s sequence (causal, temporal, chronological, semantic) and then measured how these corresponded with participants’ recall. Causal : describing the events in order of which cause-and-effect occurred E.g., scene A caused scene C, therefore we will describe scene A and scene C subsequently Temporal : describing the events in which they were shown in our visual timeline E.g., scene A was shown before scene B and scene C, so we will describe scenes A, B, and C in that order Chronological : describing the events in order of which they happen in the story’s timeline E.g., scene A happens before scene C which happens before scene B, so we will describe the events in order of scene A, then C, then B Semantic : describing the events based on how similar their storylines were to each other E.g., scene B and C are showcasing the same idea of the main character describing his impairment, therefore we will describe them together Through their paradigm, they found that causal and chronological strategies of recollecting the events better predicted the overall memory for the film compared to the other strategies. Even when participants were asked to describe the film in temporal or chronological order, the causal strategy persisted. These results indicate that when humans recall a series of events, they are oftentimes organizing their thoughts in a cause-and-effect manner. What aspects of event memories are impacted with aging? – Curb Your Enthusiasm Movies aren’t the only form of media that have been used in cognitive neuroscience studies. In a similar manner, sitcoms have been used to measure memories for events. The hit TV series Curb Your Enthusiasm  was viewed in Delarazan et al. (2023)  by young adults and older adults in order to assess human memory in aging. These two groups were then tested on two forms of memory, one that was narrative (using words) and one that was perceptual (using images). Older adults were worse with the perceptual memory task compared to younger adults. This was especially true when it came to recognizing events that were similar to the visuals they were presented with in the episode, but not actually included. Since there was no difference in the narrative form of recall, this study provides evidence for perceptual aspects of memories being more vulnerable to aging in human subjects . The media-watching paradigm: future directions and implications An interesting new direction neuroscientists can take, that seemingly intersects all of these prior findings, is further analyzing how emotions are playing into these effects. Wallace et al. (2025) and Antony et al. (2021) both indirectly highlight this idea. Through the multisensory experience enhancing memory in the former and surprise enhancing memory in the latter, we see that the viewer’s internal experience seems to influence whether they correctly recall events, even if they are not fully aware of it. Specifically looking deeper into how dopamine levels fluctuate during a media-watching experience, particularly throughout various types of media genres, can highlight how memories for events are enhanced or impaired automatically. This new and upcoming paradigm has made for more enjoyable research visits for participants while also holding integrity for how individuals would naturally recall events. Therefore, through all of these various media-watching studies, we are closer to answering scientific questions surrounding human memory in a more effective and enjoyable way than ever before. References Antony, J., Lozano, A., Dhoat, P., Chen, J., & Bennion, K. (2024). Causal and Chronological Relationships Predict Memory Organization for Nonlinear Narratives. Journal of Cognitive Neuroscience , 36 (11), 2368–2385. https://doi.org/10.1162/jocn_a_02216 Antony, J. W., Hartshorne, T. H., Pomeroy, K., Gureckis, T. M., Hasson, U., McDougle, S. D., & Norman, K. A. (2021). Behavioral, Physiological, and Neural Signatures of Surprise during Naturalistic Sports Viewing. Neuron , 109 (2), 377-390.e7. https://doi.org/10.1016/j.neuron.2020.10.029 Delarazan, A. I., Ranganath, C., & Reagh, Z. M. (2023). Aging impacts memory for perceptual, but not narrative, event details. Learning & Memory , 30 (2), 48–54. https://doi.org/10.1101/lm.053740.122 Wallace, R. S., Mckeown, B., Goodall-Halliwell, I., Chitiz, L., Forest, P., Karapanagiotidis, T., Mulholland, B., Turnbull, A., Vanderwal, T., Hardikar, S., Gonzalez Alam, T. R., Bernhardt, B. C., Wang, H.-T., Strawson, W., Milham, M., Xu, T., Margulies, D. S., Poerio, G. L., Jefferies, E., … Smallwood, J. (2025). Mapping patterns of thought onto brain activity during movie-watching. eLife , 13 , RP97731. https://doi.org/10.7554/eLife.97731

Alexa Kightlinger As a researcher, I’ve always been interested in how memory can be altered, particularly how stress or fear plays a part in it. As I’ve discussed in previous articles, episodic memory may not always be rooted in truth. Eyewitness accounts can be altered by various factors that play into how much attention we pay to a situation. While it’s easy to understand how the amount of attention we pay to a scene or whether we are tired may impact the details we remember, not much is known about how dissociation impacts our memory. As we will discuss, dissociation is often caused by individuals experiencing traumatic events. It’s amazing what the body will do to protect the brain from negative memories. It is my hope that this article shines a light on just one small aspect of what those who experience trauma may face.  Dissociation is a complex psychological concept where the individual experiences a disconnect from reality. As a key feature of dissociative disorders, dissociation is often brought on as a result of chronic developmental stress as patients diagnosed with this disorder report higher frequencies of childhood abuse or neglect (Șar, 2014). As it is with most disorders, dissociation falls along a continuum, with dissociative identity disorder (DID) on the most severe end. Those who suffer from dissociative disorders may experience disruptions in one or more mental functions, affecting areas of one’s memory, identity, or consciousness. The DSM-5 (2013) breaks dissociative disorders into five categories. (1) Dissociative Identity Disorder Diagnostic Criteria A: The possession of two or more distinct personality states which results in the disruption of identity. B: Recurring gaps in recalling everyday experiences. C: Stress in social, occupational, or other social areas of functioning. D: Disturbances that are not a normal part of cultural or religious practice.  E: Symptoms that can not be attributed to physiological effects of substances or other medical conditions. (2) Dissociative Amnesia Diagnostic Criteria A: Inability to recall important autobiographical information. B: Stress in social, occupational, or other social areas of functioning. C: Symptoms that can not be attributed to physiological effects of substances or other medical conditions. D: Disturbances that can not be explained by DID, PTSD, acute stress disorder, somatic symptom disorder, or major / mule neurocognitive disorder. (3) Depersonalization/Derealization Disorder Diagnostic Criteria A: Presence of persistent depersonalization and/or derealization events. B: Reality testing remains intact during depersonalization and/or derealization events. C: Stress in social, occupational, or other social areas of functioning. D: Symptoms that can not be attributed to physiological effects of substances or other medical conditions. E: Disturbances can not be explained by other mental disorders such as schizophrenia. (4) Other Specified Dissociative Disorder While similar to other categories, other specific dissociative disorders are used in situations where the clinicians find that the presentation of the disorder does not meet the full diagnostic criteria for any specific dissociative disorder. (5) Unspecified Dissociative Disorder. The unspecified dissociative disorder is used when the clinician chooses not to specify reasonings that criteria are not met; similar to situations in which there is not enough information to make a specific diagnosis, like in an emergency room setting.  Out of Body Experiences  As mentioned before, dissociation is frequently reported among individuals who experience high levels of stress and trauma at a young age. It often develops to help individuals cope with the trauma or stress by disconnecting them from distressing thoughts or emotions. Many report having an “out of body” experience where they are almost like an observer of the event that is occurring. These usually occur when individuals are placed in near death situations and are commonly associated with psychiatric disorders, brain dysfunction, and pharmacological agents   (Madgal et al., 2021). While few cases have been reported alongside a DID diagnosis, a 15-year-old male patient who described experiencing this strange phenomenon was later diagnosed with DID and dissociative fugue (Madgal et al., 2021). Doing so allows the individual to develop an emotional numbness. While this does help prevent individuals from becoming overwhelmed by emotions, prolonged dissociation may lead to cognitive challenges or confusion with maintaining a sense of self. In some cases, dissociation may even become a natural response when individuals are placed in non-threatening situations. Treatment Dissociative disorders are often difficult to diagnose, leading many cases to go undiagnosed or misdiagnosed. It is estimated that approximately 7% of the population may have suffered from a dissociative disorder at one time in their life (Mental Health America, 2025). While no medication has been found to specifically treat dissociation, many are prescribed antidepressants, which address the anxiety and mood symptoms that are comorbid with this disorder (Gentile et al., 2013). Psychiatrists must approach dissociative disorders with caution since medications such as benzodiazepines can reduce anxiety, but worsen dissociation. For individuals with DID, some have found success in the following: Selective serotonin reuptake inhibitors  Tricyclic antidepressants Monoamine oxidase inhibitors  Beta-blockers Clonidine Anticonvulsants Benzodiazepines *Note that while one medication may have worked for one person, it is important for clinicians to approach each case separately. In addition to medication, specialized therapy is another choice individuals choose to pursue. Facilities, such as what is offered at The Chicago Psychoanalytic Institute Treatment Center, offer a safe environment to facilitate emotional healing. By focusing on aspects of exploring underlying trauma, emotional awareness, developing coping mechanisms, and improving interpersonal relationships, clients can work towards healing (Chicago Psychoanalytic Institute, 2024). Several techniques may be taught to help someone suffering from a dissociative disorder heal. Subramanyam et al., (2020) outlines a few treatment methods clinicians may employ to help their client heal from trauma.  Psychoeducation : Focuses on normalizing the individual's symptoms and relating them to the dysfunction they experience in daily life. This helps shift focus away from victimization and allows them to understand themselves by giving meaning to their symptoms. Grounding Skills : By helping the patient detach from emotional pain, patients are taught to shift their attention from negative emotions to external cues in the present.  Cognitive Awareness:  The patients ask cognitively oriented questions such as “Where am I?” or "What day is it?” Sensory Awareness:  Similar to grounding skills, patients are taught how to use their senses to anchor them to the present moment. Distress Tolerance:  This teaches the patient to tolerate negative emotions by increasing their capacity to handle painful emotions when the situation cannot be changed immediately. This helps eliminate negative behaviors like substance abuse.  Impact Dissociation not only affects the individual but also their close friends and family. Memory lapses can make conversation difficult when the individual suffers from dissociation and can not remember important information, leading to disruptions in family routines or minimizing time families originally had for leisure (Mohammad et al., 2023). This can also cause frustration and anger if friends and family members are not understanding or supportive of what their loved one is dealing with. Severity can also lead to an increased load of responsibilities as severe dissociation can interfere with daily life. Caregivers may be tasked with reminding individuals of daily tasks/important events or helping them with emotional regulation during stressful times. Additionally, the lack of awareness of how dissociation can impact all involved contributes to misunderstandings and stigmatization. For more severe disorders such as DID, the media has misrepresented them as violent and dangerous, leading others to view them as the curator of violence, rather than the victim of it. Conclusion I hope this article has provided more information not just on what dissociation is, but the effect it has on others. Furthering our understanding of dissociation helps promote awareness of this mental health challenge. Regardless of whether we are personally affected by this or not, educating ourselves helps bridge the gap between the unknown and fosters an air of understanding and empathy towards those who experience dissociation as part of their everyday lives. References American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders  (5th ed). Pearson. Dissociation and Dissociative Disorders . (n.d.). Mental Health America. https://mhanational.org/conditions/dissociation-and-dissociative-disorders Dissociation: Understanding Its Complexities and Healing - Chicago Psychoanalytic Institute . (2024, December 6). Chicago Psychoanalytic Institute Treatment Center. https://chicagoanalysis.org/blog/conditions-and-diagnoses/dissociation-treatment/ Gentile, J. P., Dillon, K. S., & Gillig, P. M. (2013). Psychotherapy and pharmacotherapy for patients with dissociative identity disorder. Innovations in Clinical Neuroscience , 10 (2), 22. https://pmc.ncbi.nlm.nih.gov/articles/PMC3615506/ Mohammad, Y., Kumar, R., Sinha, N., & Kumar, P. (2023). A study of stressors, family environment, coping patterns, and family burden in persons with dissociative disorder. Industrial Psychiatry Journal, 32 (2): 317-322. https://doi.org/10.4103/ipj.ipj4223   Mudgal, V., Dhakad, R., Mathur, R., & Sardesai, U. (2021). Astral projection: A strange out-of-body experience in dissociative disorders. Cureus, 13 (8), 17037. https://doi.org/10.7759/cureus.17037 . Şar, V. (2014). The many faces of dissociation: Opportunities for innovative research in psychiatry. Clinical Psychopharmacology and Neuroscience , 12 (3), 171–179. https://doi.org/10.9758/cpn.2014.12.3.171

By Harshil Vijayan, B.A., RBT Let us analyze and discuss one of the most controversial questions of all time: How old are you? This question has the power to make a room go quiet and fill a face with disgust. The social norm regarding age is simply not asking about it. But why? What is the cause of social stigma around one's age? Is it the fear of being closer to death? Is it an indication of one's beauty and fitness? Whatever the reason for the stigma, it truly clouds the meaning of that double-digit number. Your age should be a celebration of the amount of time you have persevered on this planet, not an embarrassment. Now, this is easy for me, a 23-year-old, to say, but I am here to explore ways to help people love their age. An important concept to understand is that your chronological age (the number of days since birth) differs from your biological age (the functionality/wear and tear of your cells, tissues, and organs). The main difference between the two is that chronological age is not malleable, while biological age depends on how you care for your health. One can be chronologically 50 years old and simultaneously feel biologically 60 years old, but the same chronologically aged people can feel 40 or even 35 biological years old. Genetics can impact your biological age, but your actions can help decrease it. One of these actions is the amount of physical activity you partake in (Østhus et al., 2012); genetics gives you the poker hand, and you decide how you want to play that hand based on the situation. Is it our chronological age that has been scaring us, or is it really the effects of biological aging that raise our fear? The good news is that we can control one of them. The Taker of Experience One of the most daunting aspects of aging is its associated diseases, and I want to talk about one that affects 13.8 million people aged 65 and older (Rajan et al., 2020). Alzheimer's Disease (AD). While studying age-related diseases, AD felt the most painful to learn about. Sixty-five years of life for any person is filled with countless memories formed, connections made, emotions felt, and sights seen. The concept of experiencing a degeneration that eliminates all of these magical revelations from memory strikes me as quite preposterous; should we not relish all of these experiences at the end of our lives? Current medicine has it so that when AD is diagnosed, the disease will most likely have spread throughout the brain, and unfortunately, some can only watch their loved ones slowly lose the realization of the things they once knew. There is only limited research supporting the complete elimination of AD, but we can still think optimistically, knowing that there are ways we can delay the development of this disease. Inevitable for some…maybe, but the ability to delay…definitely. The Alzheimer's Association describes dementia as a "general term for loss of memory, language, problem-solving and other thinking abilities that are severe enough to interfere with daily life." Dementia can come in multiple forms, for example, vascular, Lewy body, or frontotemporal dementia, but the most common type of dementia is Alzheimer's disease. AD is a "degeneration of the brain," leading to the difficulty of remembering new information and progressive memory loss. On average, people with AD will start to see symptoms around their mid-60s and get diagnosed at the same time. Unfortunately, there is no cure in this story. Most people and their families can get extremely discouraged after a diagnosis, but the beauty of the human heart is that there is always hope and perseverance available to get back up and battle against this disease. Of course, many treatment plans can aid the quality of life after diagnosis, but how sustainable is this? The burning question is, 'When should we take action to fight this disease of aging?' I wrote this paper because of the discovery of people's responses to a diagnosis. For example, people who drink alcohol and smoke tobacco tend to decline in these harmful activities after a cancer diagnosis (Pinto et al., 2005), but how can we enforce this decline without having to go through the horror of a cancer diagnosis? The unfortunate situation with Alzheimer's is that by the time of diagnosis, multiple parts of the brain will have already gone through atrophy and degeneration (da Silva Filho et al., 2017). Indeed, it is never too late to start trying treatments to get better, but in this case, we should begin as soon as possible. Even if one gets diagnosed around 65 years old, the neuropathologic hallmarks (characteristics of the disease) of AD can start developing decades earlier in the brain; the most common hallmarks are amyloid beta plaques and neurofibrillary tangles (NFTs) (Porsteinsson et al., 2021). How quickly these hallmarks start developing can be traced back to genetics. The apolipoprotein E (APOE) gene is one of the major genes influencing AD development; this gene comes in three variations—known as alleles—e2, e3, and e4 (Liu et al., 2013). When you are born, you inherit one out of six combinations of any two of these three alleles—one from each parent. For example, you could have e2/e2, e2/e3, e4/e3, …etc. Holding more copies of the e4 allele has been found to accelerate AD development, while holding more copies of the e2 allele has been found to delay the development of AD (Yamazaki et al., 2019). Now we know that if you are born with more e4 alleles, you have a higher chance of developing those neuropathological hallmarks early. What is the point of knowing this, you may be asking? In terms of AD development, genetics plays a huge role in how our biological age can increase or decrease across the lifespan. It makes sense to feel dispirited when given such unlucky odds; how do you win with a poker hand with such a low chance of winning from the start? How can you combat this early development of amyloid beta plaques and NFTs when you were born with this disadvantage? Luckily, in the famous nature vs nurture argument, nature (genetics) does not take the whole cake. We can use the environment to our advantage. If given a horrible poker hand, we can still read the room and other people's actions to help land us in an extraordinary situation. Do not let genetics define your age. Let physical activity show you the path to youth. This image displays a brain scan highlighting amyloid beta plaques in both positive and negative diagnoses of Alzheimer's disease. The positive scan illustrated the extent to which the amyloid plaques have accumulated at the time of diagnosis. Movement Is The Medicine One of the most significant complications in the world of healthcare and medicine is the high cost of treatment in the United States. Even trying to eat healthier can come with a rise in costs, but fear no less: physical activity is a free treatment for many age-related diseases. A handful of longitudinal epidemiological studies support the claim that physical activity can delay the physical and cognitive decline associated with aging (Van Gelder et al., 2004). Regular and constant physical activity has also been found to contribute to lower levels of amyloid beta plaques and NFTs—this is due to the reduced hyperphosphorylation of the tau protein from physical activity (López-Ortiz et al., 2021)—which ultimately delays the arrival of Alzheimer's disease. When is the deadline for gaining all the benefits from physical activity? Never. Physical activity has been found to slow the cognitive decline associated with dementia across the whole age spectrum (Ahlskog et al., 2011). Even though the physical activity homework assignment is not due until your death day, the assignment will require some thoughtful effort. Interestingly, in this case, the more you do your assignment, the more you will extend your due date.  The type of physical activity that prevents AD is called aerobic physical activity, a rhythmic physical activity that utilizes more oxygen by increasing your heart rate—such as walking, jogging, and swimming. Now, for the million-dollar question. How much physical activity? One study states that being physically active for older adults—ages 65 and above—means they are aerobically exercising for a minimum of 30 minutes/day for 5 days/week. Maintaining this routine of physical activity has been found to help older adults maintain their cognition (De la Rosa et al., 2020). Even younger people who are carrying the APOE e4 alleles benefit from partaking in this physical activity; adults around 50 years old with the e4 allele were to have more amyloid beta loads if they were consistently physically inactive (Tokgöz et al., 2021). You can continually improve your brain pathology with physical activity regardless of age. I have just described a free, indispensable technique available to everyone to battle an age-related disease that does not have a medical cure, so why do people still live sedentary lives? One study found that the main reason why older people are not physically active is simply because there is a lack of interest; physical inability is the second biggest reason (Crombie et al., 2004). Trying to help people care about their health has much to do with education, institutional policies, family background, and social stigma. We do not know what is happening in people's personal lives that may be limiting their engagement with physical activities, but we can always make these concepts more aware to the public eye. I believe many people, like me, tend to wait for a problem to occur before they start finding the solutions, but if we find the solutions before the problem occurs, we do not need to go through all of the sufferings of the problem. Finding the solutions before a problem arises is difficult, but it does not mean we need to become psychics magically; it just requires more vigilance. The Love of Growing Up Writing these blogs aims to spread awareness of the good and the bad aspects of brain health and how we can improve it for the next person. Alzheimer's is the problem, and physical activity is the solution. Looking at the bigger picture, physical activity is not just a way to delay AD but also to decrease our biological age and to feel younger. Sometimes, you lose the poker hand, but it is a good thing that a poker game has many opportunities to win. Each birthday is another opportunity to work to celebrate even more birthdays. It is an opportunity to love your age and live your life. References Crombie, I. K., Irvine, L., Williams, B., McGinnis, A. R., Slane, P. W., Alder, E. M., & McMurdo, M. E. (2004). Why older people do not participate in leisure time physical activity: a survey of activity levels, beliefs and deterrents. Age and ageing, 33(3), 287-292. da Silva Filho, S. R. B., Barbosa, J. H. O., Rondinoni, C., Dos Santos, A. C., Salmon, C. E. G., da Costa Lima, N. K., ... & Moriguti, J. C. (2017). Neuro-degeneration profile of Alzheimer's patients: a brain morphometry study. NeuroImage: Clinical, 15, 15-24. Jylhävä, J., Pedersen, N. L., & Hägg, S. (2017). Biological age predictors. EBioMedicine, 21, 29-36. Liu, C. C., Kanekiyo, T., Xu, H., & Bu, G. (2013). Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy. Nature Reviews Neurology, 9(2), 106-118. López-Ortiz, S., Pinto-Fraga, J., Valenzuela, P. L., Martín-Hernández, J., Seisdedos, M. M., García-López, O., ... & Santos-Lozano, A. (2021). Physical exercise and Alzheimer’s disease: effects on pathophysiological molecular pathways of the disease. International Journal of Molecular Sciences, 22(6), 2897. Pinto, B. M., & Trunzo, J. J. (2005). Health behaviors during and after a cancer diagnosis. Cancer: Interdisciplinary International Journal of the American Cancer Society, 104(S11), 2614-2623. Porsteinsson, A. P., Isaacson, R. S., Knox, S., Sabbagh, M. N., & Rubino, I. (2021). Diagnosis of early Alzheimer’s disease: clinical practice in 2021. The journal of prevention of Alzheimer's disease, 8, 371-386. Rajan, K. B., Weuve, J., Barnes, L. L., McAninch, E. A., Wilson, R. S., & Evans, D. A. (2021). Population estimate of people with clinical Alzheimer's disease and mild cognitive impairment in the United States (2020–2060). Alzheimer's & dementia , 17 (12), 1966-1975. Roses, MD, A. D. (1996). Apolipoprotein E alleles as risk factors in Alzheimer's disease. Annual review of medicine, 47(1), 387-400. Tokgöz, S., & Claassen, J. A. (2021). Exercise as potential therapeutic target to modulate Alzheimer’s disease pathology in APOE ε4 carriers: a systematic review. Cardiology and Therapy, 10, 67-88. Van Gelder, B. M., Tijhuis, M. A. R., Kalmijn, S., Giampaoli, S., Nissinen, A., & Kromhout, D. (2004). Physical activity in relation to cognitive decline in elderly men: the FINE Study. Neurology , 63 (12), 2316-2321.   Yamazaki, Y., Zhao, N., Caulfield, T. R., Liu, C. C., & Bu, G. (2019). Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies. Nature Reviews Neurology, 15(9), 501-518. Østhus, I. B. Ø., Sgura, A., Berardinelli, F., Alsnes, I. V., Brønstad, E., Rehn, T., ... & Nauman, J. (2012). Telomere length and long-term endurance exercise: does exercise training affect biological age? A pilot study. PloS one, 7(12), e52769.

by: Jacinda Taggett. Frankie sat across from her friend, Kieran, on an evening in the winter of 2021. The two were having a conversation about Frankie’s current state, which had been abnormal. Frankie was currently undergoing a psychotic episode, and her cognition displayed impairments during their talk. Randomly, when prompted a question, Frankie would lose her train of thought midway through the sentence, and lose track of the question itself. This made the conversation with Kieran difficult, as he had to continuously remind Frankie of what was going on, while she stared blankly at the countertop and was unable to stay attentive. Frankie’s time in college was more difficult during this episode, as she could not keep track of her lectures. She was convinced that her professor and classmates were listening to her thoughts, which made her wary of going to lecture. Doing assignments took longer than usual, since she would be unable to comprehend what she was reading before herself. Some of these cognitive deficits were repaired once Frankie became medicated again, but some of these features still persisted. What Frankie suffers from is a working memory deficit, common in people with psychotic features. Specifically in a disorder called schizophrenia, these cognitive deficits continue even after becoming medicated. In this article, we will be discussing the impact that working memory deficits have on individuals with schizophrenia, and how it affects their everyday life. Working Memory Working memory, as we know it today, was first proposed by Baddeley and Hitch (1974). They claimed that memory was split into two, long-term and short-term. Working memory is the official name for what we consider to be short-term memory. This type of memory is known for temporarily storing information, and manipulating it when we need to do so. It can be thought of as the mental process in which someone has to solve a math problem, remember a note before they write it down, or have the capability to drive (even without remembering the process afterwards). Working memory is particularly important for everyday tasks, such as maintaining a conversation or being able to recall where an item was placed just moments before. When working memory becomes impaired, it becomes difficult for people to function normally. Schizophrenia One of the most misunderstood neurological disorders is schizophrenia, which is a disorder that is characterized mostly by its prevalence of hallucinations and delusions. It is oftentimes confused with dissociative identity disorder, previously known as multiple personality disorder. Other times, even when correctly identified by the general public, individuals with schizophrenia are considered dangerous or suspicious people. Schizophrenia is a debilitating mental disorder, which typically causes more suffering and harm for the specific individual rather than the people around them.  According to the Diagnostic and Statistical Manual of Mental Disorders  (5th ed.; DSM–5; American Psychiatric Association, 2013), individuals must have at least one positive symptom and one or more other symptoms (either positive or negative) for at least a month, and general disturbance in everyday life for over 6 months. Positive Symptoms Characterized as either psychotic or disorganized symptoms, positive symptoms of schizophrenia are the most notable part of the disorder. Psychotic symptoms include hallucinations and delusions. Hallucinations are when an individual experiences an activation of their senses (i.e., sight, hearing, touch, etc.). An example of hearing a hallucination is if you were to be sitting in a quiet library and then hear a voice telling you “Go to that shelf” when no one in person is addressing you. Delusions, on the other hand, are beliefs that are not perceived in reality. These beliefs also typically affect everyday living significantly, like how Frankie’s delusion of everyone reading her mind impacted her education. Disorganized symptoms often involve thought, speech, and behavior of an individual. Oftentimes, these would appear as an inability to communicate properly, and have the individual speak like a broken robot, randomly generating words. This condition is deemed “loose associations” and often impairs the individuals’ thoughts. Disorganized behavior is another positive symptom of schizophrenia, which makes it difficult for an individual to begin or finish tasks. Negative Symptoms The negative symptoms of schizophrenia are often the emotional and social aspects of the individual. These symptoms include a lack of emotional expression or feeling (i.e., happiness or motivation), and minimal socialization or communication. Cognitive Deficits Cognition that is affected by schizophrenia include attention, processing speed, memory (both long-term and short-term), and learning. These deficits typically impact an individual’s everyday life without them being aware of it occurring. Working memory will be the focus of this article, as it usually encompasses all aspects of cognitive functioning listed previously. Cause of Schizophrenia Although the direct cause of schizophrenia is unknown, the main hypothesis for decades has been that the neurological basis is an imbalance of dopamine in the brain. Dopamine is one of the most well-known but reasonably misconceived monoamine neurotransmitters (a neuron’s set of keys) in psychological and neuroscientific discourse. Commonly known as the “pleasure neurotransmitter”, it has been shown to not only be involved in reward and motivation, but also with movement and learning as well. The main idea behind schizophrenia’s cause, termed the “dopamine hypothesis”, is that hyperactivity of the inhibitory dopamine receptors (the neighboring neuron’s lock that dopamine binds to) leads to positive symptoms and hypoactivity of the excitatory dopamine receptors leads to the negative symptoms (Davis et al., 1991, as cited in Howes & Kapur, 2009). Although this is the main hypothesis, the disorder itself is not well understood. The main evidence behind this hypothesis is that medications affecting the dopaminergic levels in the brain tend to work for schizophrenia’s positive symptoms. WORKING MEMORY IN SCHIZOPHRENIA Working memory is one of the cognitive functions that is impaired in schizophrenia, with little explanation as to how or why. Although some research indicates that dopaminergic regions in the brain are correlated with working memory function (Landau et al., 2009), there is still no effect of antipsychotic medications helping to repair schizophrenia’s deficit in immediate working memory (Mori et al., 2004). Perhaps the mindset of the individual is also involved? In a recent study by Sanchez-Torres et al. (2022), researchers assessed the cognitive abilities of schizophrenic individuals along with their symptomatology. They saw that higher scores on the Frankfurt Complaint Questionnaire, a subjective assessment of schizophrenic and psychotic symptoms, predicted lower performance in working memory neuropsychological assessments. No matter the cause, working memory impairment in schizophrenic individuals is a real problem that needs to be addressed in order to further make an impact on this population. In the next few paragraphs, we will be going over recent research done on solidifying the working memory deficits in schizophrenia patients. Trail Making Task A paradigm of working memory is the Trail Making Task, which is split into two parts (Part A and Part B). In Part B, participants are given a piece of paper with circles, each with either a number from 1-12 or a letter from A-L, making 24 circles in total. Each participant has to make a trail with their pencil (without removing it from the paper) to a sequence that goes 1-A-2-B-3-C, etc., and the assessment is shown as the time it takes to complete the task. With higher time being representative of impairment, the task indicates working memory, because you must keep track of the past two circles in your sequence in order to make a correct move onto the next one. When schizophrenic individuals complete this task compared to controls, Zanelli et al. (2022) found that patients with schizophrenia exhibited lower working memory performance that only got worse over time. Updating and Maintenance Paradigm Another paradigm, which Gotra, Keedy, and Hill (2022) claimed to be an “Updating and Maintenance Paradigm” is another indicator of working memory. In this experiment, a participant is shown a target item (i.e., purple square) in a specific location on a grid, followed by a delay from 1000-8000 ms. Then, they are shown a comparison item (i.e., blue square) located somewhere on the grid, without the purple square present. Participants must indicate whether the comparison item was in the same location as the target item, and their accuracy is a measure of their working memory capability.  As delay increased during this paradigm, performance decreased for individuals with schizophrenia spectrum disorder compared to controls, and an even greater decline when the delay was higher. These results concluded that working memory is short-lived and subject to interference in individuals with schizophrenia. WHY THIS MATTERS As discussed before, working memory is essential for day-to-day functioning. Given that the onset of schizophrenia begins during college years (ages 18-25), research can further ensure that working memory can be repaired in the schizophrenic individuals to aid their academic success and help them achieve their goals. Capability to maintain a professional or educational life can be difficult for individuals with schizophrenia, as their ability to communicate and problem-solve is impaired. In a recent study by Dickson et al. (2020), schizophrenic individuals are less likely to complete secondary or higher education, and overall have lower academic achievement.  Before we can improve the lives of these individuals, more research needs to be done on the different types of learning and memory, especially ones that can be applicable to real-world and educational environments. To add on, more studies should be done on the learning and memory for human subjects currently experiencing symptoms of psychosis. Although the ethical and conventional approaches to this are limited, it would be beneficial to aid schizophrenic patients during episodes instead of only when they are medicated. While considering medication, more research needs to be done on varying antipsychotics and their effects on cognition, given the conflicting literature. With this research can we establish other medication routes that will improve the cognitive deficits in schizophrenia? Until all of these gaps are filled in the field, we cannot create the difference that we strive to make in individuals with schizophrenia. REFERENCES American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596 Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine in schizophrenia: A review and reconceptualization. The American Journal of Psychiatry, 148 (11), 1474–1486. https://doi.org/10.1176/ajp.148.11.1474 Dickson, H., Hedges, E. P., Ma, S. Y., Cullen, A. E., MacCabe, J. H., Kempton, M. J., Downs, J., & Laurens, K. R. (2020). Academic achievement and schizophrenia: a systematic meta-analysis.  Psychological medicine, 50 (12), 1949–1965. https://doi.org/10.1017/S0033291720002354 Gotra, M. Y., Keedy, S. K., & Hill, S. K. (2022). Interactive effects of maintenance decay and interference on working memory updating in schizophrenia. 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Assessment of cognitive impairment in psychosis spectrum disorders through self-reported and interview-based measures. European Archives of Psychiatry and Clinical Neuroscience, 272( 7), 1183-1192. https://doi.org/10.1007/s00406-022-01399-4 Zanelli, J., Reichenberg, A., Sandin, S., Morgan, C., Dazzan, P., Pilecka, I., Marques, T. R., Morgan, K., Young, A. H., & Mollon, J. (2022). Dynamic and static cognitive deficits in schizophrenia and bipolar disorder after the first episode.  Schizophrenia Bulletin, 48 (3), 590-598. https://doi.org/10.1093/schbul/sbab150