Post-Midterm Lecture Notes

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Autism Part 1 - Controversy on the causes and treatments of Autism, and the classification of Autism as a disorder - Autism spectrum disorders are on average 80% reliant on genetic causes, so environmental causes are about 20% of the causes Autism Myths: 1. People with Autism do not want friends a. This is false. Those with Autism struggle with social skills and therefore have difficulties interacting with peers. 2. People with Autism can’t feel or express emotions a. Autism doesn’t make an individual unable to feel emotions, it makes them communicate and perceive emotions in different ways 3. People with Autism can’t understand the emotions of others a. Autism impacts an individual's ability to understand unspoken communication 4. People with Autism are intellectually disabled a. Autism often brings many exceptional abilities and talents What is Autism? - DMV-5 used to diagnose Autism - OCD is a comorbid condition of Autism, overly focused interests and obsessions with certain things - Overly sensitive to sensory input, especially noise - ASD is polygenic, not single risk factor, at the association level of genetics

Early signs of Autism (6 - 12 months) - Limited smiling when approached by caregivers - Not necessarily comforted by caregiver’s presence - Delayed babbling, sign of disrupted speech - Does not respond to their name - Poor eye contact - Rarely seeks attention, satisfied entertaining themselves - Does not gesture to communicate by 10 months - Autism is a spectrum, these are generalities Children are reliably diagnosed as young as 24 months, but the median age is older than 4 years old - Parents can not reliably be experts on noticing ASD behavior Public opinion on Autism: - Vaccines (that contain mercury) can cause autism by damaging intestinal lining of the child which compromises the protection of the digestive system and therefore damaging neurons ASD Genetic Mechanism: - Polygenic inheritance, Polygenic traits - Changes in over 1000 genes associated with ASD, but these associations lack specificity and causation - Most gene variations have only a small effect, and can combine with environmental risk factors - Non-genetic factors may contribute to about 30-40% of ASD risk - Many genes associated with ASD are involved in brain development - Inheritance pattern is unknown, but tends to run in families - Environmental factors include parental age, infections of the mother - Why do we talk about brain development? - The proteins produced from these genes affect multiple aspects of brain development - These genes coming together impact production, growth, and organization of neurons - Polygenic traits impact dendrites - Some studies indicate that those with ASD have more neurons during brain development

ASD: Commonly Implicated Genes: - SYNGAP1: gene provides instructions for making a protein called SynGAP - Plays an important role in nerve cells in the brain - Found at the junction between nerve cells (synapses) where cell-to-cell communication takes place - DYRK1A: gene provides instructions for the enzyme that is important in the development of the nervous system - The proteins whose activity the DYRK1A enzyme helps regulate are involved in various processes in cells, including cell growth and division and the process by which cells mature to carry out specific functions - SHANK3: gene provides instructions for making a protein that is found in many of the body’s tissues, most abundant in the brain - SHANK3 protein plays a role in the healthy functioning of synapses - Connections between nerve cells where cell to cell communication occurs - CHD8: gene provides instructions for making a protein that regulates gene activity by a process known as chromatin remodeling - Helps to control the amount of neurons in the brain with the objective of preventing overgrowth - Chromatin is the complex of DNA and protein that packages DNA into chromosomes. Chromatin can be changed to alter how tightly DNA is packaged - CHD8 protein is thought to affect the expression of many other genes that are involved in the brain development before birth ASD Terms: - Synaptogenesis: The rapid expansion in synaptic formation in order to deal with the bombardment of sensory input - During infancy, brain is flooded with sensory input that is hard to organize, Synaptogenesis helps the brain deal with sensory input - Synaptic Pruning: reduction in the number of synaptic connection which enables more efficient synaptic configurations (more efficient, supports ongoing learning) - We do not need unnecessary synapses - Brain Adaptation (Connections not used): are pruned as they are no longer needed, preventing unnecessary connections that slow the brain down

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- Early brain overgrowth - Due to prenatal cell cycle deregulation, causes over-abundance of cortical neurons, leads to disrupted neural network development and disrupted function - Evidence that ASD begins in the womb Autism: Brain Imaging Study: - Brain Pathology Studies: - 67% overabundance of brain cells in frontal region - Excess number of neurons: - Too many incorrect connections - Miswiring of brain network - Slowing down of frontal brain regions - Decreased synaptic pruning in frontal regions to explain executive dysfunction Normal Pruning: - Genetic differences in Autism are linked to lack of synaptic pruning - Helps the brain to specialize and become more complex, accurate - Volumetric loss in the basal ganglia and the cerebellum (balance and coordination) Cerebellum & Autism - Abnormalities of cerebellar function in autism are associated with deficits in motor behavior → Difficulty executing appropriate behavior Autism & Stimming: - Self-stimulatory behavior also known as stimming and self-stimulation - The repetition of physical movements, sounds, words, or moving objects

- Form of communication - Self soothing mechanism Autism Part 2 fMRI Autism Study: - More activation does not mean more accuracy - Individuals w Autism presented with photos human faces and neutral pictures of objects in fMRI - Compared activation in fusiform gyrus between faces and neutral objects and words - Study showed that the fusiform gyrus was activated, but that it is misused to read words or look at neutral objects Q: What did fMRI give us that we didn’t know before? - Before it could be concluded that Autism patients’ fusiform gyrus was not activated when observing faces, but that is a misconception - Other interpretations besides misuse: - Processing is less efficient in reading, and people with autism require more visual resources to perform a task, hence visual centers are used for object recognition and reading, therefore, recruiting the fusiform gyrus is actually helping those with autism Mirror Neurons: - Concept originated from the observation of neurons in the frontal cortex of the monkey - Helped advance discussions on social cognition - Mirror neurons not activated at rest, but activated during motor movement - Also activate when the monkey observes motor movement - There is not a brain basis for how we interpret the actions of others, and can explain a lack of imitation, reduced joint attention - In Autism, there are resting mirror neurons when they should be activated Brain & Empathy: Right Supr-Marginal Gyrus: - Involved in perception of space, identifying postures and gestures of other people, therefore important to mirror neurons - Damage to this area is associated with impaired empathizing, empathy requires an understanding of other - Damage implicates reduced compassion - Lack of self-consciousness such as guilt or embarrassment

EEG: Mu Rhythm and Autism: - The mu rhythm is present when the body is at rest - Mu rhythm is suppressed or blocked when the person performs a motor action - Suppressed when the person views another or visualizes a motor action - Mu is impaired in individuals with Autism → does not suppress Interventions: - Speech therapy is a front-line intervention Theory of Mind: - Influential when talking about Autism, because theoretical frameworks give us a way to look at Autism Applied Behavior Analysis (ABA): - Gold standard for Autism treatment - Reverse social deficits in Autism - Social stories designed to help individuals with Autism learn subtleties of social interaction Neurochemistry of Social Bonding - Oxytocin: - Hormone & Neuropeptide (neuronal signaling molecules) - Produced in the hypothalamus and released in the pituitary gland - Plays a role in social bonding Autism Co-occurring Conditions: - ADHD → most common co-occurring condition w/ Autism - Easy for clinicians to miss the ASD diagnosis in children with ADHD Autism & Learning Disabilities: - Dyspraxia: affects motor skills - Dyslexia: affects language processing - Lack of recruitment of brain regions - Activation found in unusual places - Dysgraphia: affects writing abilities - Dyscalculia: affects ability to do math - Intraparietal Sulcus, decreased gray matter density Learning Disabilities & Brain: - Reduced dendritic growth - Reduced myelination

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- Reduced production of glia Diffusion Tensor Imaging Study: - Brain’s white matter was involved in the efficient processing of sound information in to the lower levels of the brain - Brain scans showed a greater volume of white matter in the auditory regions known as Heschl’s gyrus for fast learners - This is where sound is processed Addictions DSM-5: Diagnostic Criteria: Addictions: - Addictions are chronic relapsing psychiatric disorders - Characterized by compulsive and loss of control for use of a drug/substance - Causes maladaptive functioning and destructive outcomes - Circuit: Frontal dysfunction (inability to override an automatic response/compulsion) - Genetic factors = approx. 40-60% of addiction causes

Liking vs. Wanting: - Liking decreases overtime - Wanting increases overtime - Important distinction in addiction science - Some people that struggle with addiction don’t even like the substance they’re addicted to, addiction takes away the choice When Neurotransmitters do not work: - Neurons might not manufacture enough a particular neurotransmitter - Too much of a particular neurotransmitter may be released - Too many neurotransmitters may be deactivated by enzymes - Neurotransmitters may be reabsorbed too quickly Dopamine (Excitatory): - Dopamine plays an important role in the coordination of body movements - Also involved in reward, motivation, and addictions - Several types of addictive drugs increase dopamine levels in the brain - Parkinson’s disease, which is a degenerative disease that results in tremors and motor movement impairments, is caused by the loss of dopamine-generating neurons

- Substances of mis-use trick the brain’s reward system - Ex: Heroin - The way the brain signals pleasure is by releasing dopamine, positive thing when through natural outlets, like eating good food, exercise - With synthetic dopamine, the brain develops a tolerance, which changes the dopamine receptor site availability, so the brain needs heroin to receive pleasure Addiction Dopamine Pathways: - Mesolimbic Dopamine Pathways: The first major dopamine pathway - Pleasure and reward seeking behaviors, addiction, emotion, perception - Mesocortical Dopamine Pathways: The second major pathway - Cognition, memory, attention, emotional behavior, and learning - The release of dopamine into the nucleus succumbence is what regulates incentive salience (the desire for achieving rewarding stimuli) - These pathways learn to continue expecting the level of dopamine associated with addictive drugs like heroin - VTA: structure in the mid-brain that sends dopaminergic neural projections to both pathways - Origin of dopaminergic cell bodies - Addictive drugs, such as alcohol give the brain a shortcut to the reward system by flooding the nucleus accumbens with dopamine (2 - 10 times more dopamine than natural sources), more quickly and reliably than natural dopamine sources, which is why addiction is so challenging to treat - Overtime, a tolerance is built (adaptation to the effect of the drug) - Therefore, dopamine has less of an impact, so the drug itself no longer gives the brain the pleasure that it use to, so more for the drug is needed more frequently to achieve the same high Differential Diagnosis (Schizophrenia): - A challenge of diagnosing addiction is being mindful that some of the symptoms that are hallmarks of schizophrenia can also show up in addiction - Tactile hallucinations involve an abnormal or false sensation of touch, perception, and movement - Associated with schizophrenia and the use of specific drugs - Examples: - Methamphetamine induced Psychosis - Can produce paranoia, anxiety, and delusions of grandeur - Easy to mis-diagnose an ecstasy induced psychotic episode with schizophrenia

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- Can produce terrifying visions or tactile hallucinations - Parasitosis: seen in high frequency in an ecstasy high or meth use leads to people feeling like bugs are crawling under the skin - Significant skin picking, skin infections, sterilization issues, byproducts - Similar to what is seen in schizophrenia - Important to ask about addiction history before diagnosing schizophrenia Addiction and Tactile Hallucinations: Pathophysiology: - Somatosensory Cortex: processing somatic sensations that arise for receptors throughout the touch that percept touch, motion, etc - How does abuse of ecstasy, cocaine, etc lead to parasitosis? - These drugs can induce rapid firing of neuronal cells of the somatosensory region of the brain leading to vivid perception of illusionary bugs on the skin - Tactile hallucinations are made possible due to faulty sensory integration of these neuronal signals in the somatosensory system Genetics and Addiction: Addiction: A1 Allele of the DRD2 Gene: - Dopamine receptor D2, also known as D2R, is a protein that is encoded by the DRD2 gene - DRD2 strongly associated with reinforcement or reward (dopamine neurotransmitter) - A1 allele of the D2 dopamine receptor gene predicts low D2 receptor availability - D2 dopamine receptor (DRD2) allele associated with substantial addiction risk - DRD2 allele results in dopaminergic deficiency - Five subtypes of dopamine receptors, but largely classified as D1 and D2 - DRD2 is strongly associated with reinforcement, A1 allele predicts low D2 receptor availability - This allele is associated with addiction risk, dopamine deficiency hypothesis - A1 allele location in a coding region that controls the synthesis of dopamine in the brain - DRD2 allele: Reward Deficiency Syndrome - Addiction = seeking synthetic means for dopamine increases (compensate for DRD2 related deficiency) Brain Behavior: DRD2 A1 Allele: - Carriers of the DRD2 A1 allele show reduced levels of dopamine receptors in the Nucleus Accumbens (Na)/ Ventral Tegmental Area (VTA) - Na/VTA: Central Regions for dopaminergic DA transmission

- Behavioral Phenotypic expression: Carriers of this allele have blunted response to rewards/ pleasurable events - When cocaine enters the brain, there is a dopaminergic surge that the Amygdala begins to associate with the drug creating a CONDITIONED response Addiction Interventions Addiction and Medication Treatments: - Why are we using drugs to treat drug use? - Harm reduction, sometimes it is unsafe for a chronic drug user to quit drugs completely until they can move safely through recovery - Suboxone : approved to treat opioid dependence - Methadone : used to treat chronic pain and opioid addiction - Antabuse : treats problem drinking by creating an unpleasant reaction to alcohol (vomiting as a strong physical deterrent to drinking alcohol, but can cause heart failure and respiratory difficulties) - Interferes with the way the body metabolizes alcohol by stopping the enzyme that processes alcohol from working

Dual Diagnosis: Addiction and Psychiatric Disorder: - A wide range of psychiatric disorders often co-occur in high frequency with addiction - Treated in specialized dual-diagnosis clinics - Drug abuse and addiction can make an accurate diagnosis of a psychiatric disorder very difficult because drugs can mask a mental illness, addiction can also make mental illness more obvious depending on the type and the addiction - Some individuals use addiction to self medicate - About 1/3rd of the people with a psychiatric disorder also suffer from addiction (NAMI) because of self-medicating and vise versa - Addiction is very dangerous when couples with depression which can lead to a downward spiral of self-medicating Addiction and Therapy: - Alcoholics Anonymous: purpose is to help all members stay sober - Non- professional, self-supporting, and apolitical intervention program - Relatability is very important Addictions by race: - Native Americans at highest addiction rate - White Americans much more likely to seek treatment - Why are these not proportional? - Access to chemical dependency programs among many reasons Neurofeedback and Addiction Treatment: - Type of bio-feedback that focuses on the brain enabling patients to change physiological activity in the form of brain waves - When the individual is focused on the pictures then the images and sounds on the computer are enjoyable, when your attention drifts or you become anxious the pictures on the computer fade in and out until your brain can focus again (neural feedback) - Repeated until individuals can control brain waves on their own - After treatment, brain inactivity decreases which is good - Can move into alpha (restful awakeness) in more natural states

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Psychiatric Disorders - Psychiatric disorders are diagnosed according to the DSM, published by the American Psychiatric Association (APA) - DSM is focused on categories - Depression is the most common mental disorder and the most common cause of disability worldwide (264m people affected) - More women diagnosed because of how depression is described in the DSM-5 - Diagnosis is highly reliant on the expertise and judgement of a clinician which is why we have categorically defined disorders DSM: Multiaxial System: - AXIS I: Clinical disorders - Disorders that are the primary clinical complaint (ie. bipolar disorder, schizophrenia, major depressive disorder) - AXIS II: Personality Disorders - AXIS III: Medical Conditions - AXIS IV: Psychosocial Problems - Ruling out stress related psychosis, grief, socioeconomic changes - AXIS V: Global Assessment of functioning - High comorbidity between depression and other disorders, someone with an AXIS II disorder can trigger and AXIS I disorder - Experience in the field is very importance because there are no lab tests so it is easy to misdiagnose - Also the only medical field where an adult can be held out of their control - 51-50: When an adult is a danger to themselves or others and needs to be kept under care - 55-85: Involuntary hold of a minor, even without their parents control Criticisms of the DSM-5 - DSM-5 diagnoses are limited descriptions which highlight deficits, weaknesses, and problems and overlook capabilities, resources, and strengths - Highly dependent on clinician’s judgement - High overlap in symptoms - Does not inform treatment specificity - Inter-rater reliability ranges from only 0.68 to 0.72 for Axis I disorders - Two clinicians can disagree on the diagnosis of the same patient

Heterogeneity of Depression: Subtypes of Schizophrenia: - Paranoid: plagued by hallucinations, often with negative messages, and delusions, both grandiose and persecutory - Disorganized: Primary symptoms are flat affect, incoherent speech, and random behavior - Catatonic: Rarely, initiating or controlling movement; copies others’ speech and actions - Undifferentiated: Many varied symptoms - Placeholder when the clinician is unsure - Residual: Withdrawal continues after positive symptoms have disappeared - DSM-5 emphasizes symptoms of biological factors Delusional Disorder vs. Schizophrenia: - Someone with delusional disorder has a fixed belief (delusion that does not change) but lacks other symptoms of schizophrenia - Delusions are non-bizarre in delusional disorder, compared to schizophrenia, but are still highly unlikely - Ex. the belief that a spouse is cheating

- Significant difference lies in functionality, impaired function is a symptom of schizophrenia, not delusional disorder Personality Disorders: group of disordered characterized by rigid, maladaptive traits that cause great distress or an inability to get along with others- - Cluster A: group of disorders characterized by odd or eccentric behaviors - Paranoid personality disorder, schizoid personality disorder, schizotypal personality disorder - Cluster B: Group of disorders characterized by dramatic, emotional, or erratic behaviors - Antisocial personality disorder, borderline personality disorder, histrionic personality disorder, narcissistic personality disorder - Cluster C: avoidant personality disorder, dependent personality disorder, obsessive-compulsive personality disorder

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Psychiatric Disorders Part 2 Borderline Personality Disorder: - “Splitting”: all good or all bad, I hate you I love you, etc - Fear of abandonment - even if the abandonment is minor or imagined. Frantic efforts to avoid being alone - A pattern of intense, unstable relationships. Quickly attaches to a new partner. Lack of boundaries. Idealizes/devalues - can’t tolerate ambiguity. - Impulsivity. Self-damaging acts. Inability to control impulsivity: shoplifting, drug abuse, spending sprees, binge eating, etc. - Emotional instability: frequent and dramatic changes in affect too short to be considered changes in mood - but “moody” - Suicidality: threats or gestures - overdose not intended to be lethal, self-mutilation; suicide notes frequently written and left in areas easily found - Persistent feelings of emptiness, guilt - Inability to regulate emotion: difficulties with anger control - cutting, slashing, burning, acts of violence - Episodes of dissociation, paranoid ideas or illusions are transient and induced by stressful external events - Disturbances of self-image/self-concept, bad or inexistent Toward an Improved Diagnostic Approach: - Bottom up approach - Bio-markers are important because they provide an objective estimate that is independent of the clinicians judgement - Helps reduce relapse rate (more depressive episodes increase the risk of relapse)

Psychiatry: Chemical Imbalances: - A chemical imbalance in the brain is said to occur when there’s either too much or too little of certain neurotransmitters in the brain - Understanding biomarkers helps reduce the stigma around psychiatric disorders - Neurochemistry is the easiest to explain to patients, compared to things like DTI, fMRI, etc. When Neurotransmitters Do Not Work: - Neurons might not manufacture enough of a particular neurotransmitter - Too much of a particular neurotransmitter may be released - Neurotransmitters may be deactivated by enzymes - Neurotransmitters may be reabsorbed too quickly A Reaction to DSM-5 Criteria: NIMH: - NIMH wants to move towards understanding disease mechanisms NIMH: The RDoC framework assumes that: 1. Mental disorders are disorders of brain circuits 2. Neuroscientific methods can identify these dysfunctions in vivo, and 3. Genetic and imaging data will yield biomarkers that can augment clinical management

Normal Brain vs. Psychopath Brain: - Decreased activity, reduced volume in the amygdala (emotion center) - Reduced amygdala correlates to reduced fear - Reduced activity in the medial prefrontal cortex (involved in decision making) Prodromal stage for Antisocial Personality Disorder: - Conduct Disorder - shown by three or more of the following: - Aggression against people or animals - Engages in frequent bullying or threatening - Often starts fights - Has used a weapon that could cause serious injury - Has shown physical cruelty to people - Has shown physical cruelty to animals - Has engaged in theft with confrontation - Has forced sex upon someone - Adults with antisocial personality disorder often had conduct disorder when they were younger Conduct Disorder Study: - 65 teenage males with CD - Compared to 27 teenage males without CD - Authors conclude amygdala and insula (perception of pain) are remarkably smaller in teens with antisocial behavior - Poor insight into others’ emotions Genetic Transmission of Psychiatric Disorders: - Genetic markers are especially important for predicting risk ENIGMA (Enhancing Neuro Imaging Genetics through Meta-Analysis: - International effort to better understand biomarkers of technology - An international effort creates much more representative results

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Psychiatric Disorders & Genetics Part 3 Genetics, Brain, and Cognition: Genome-Wide Association Study: - Involves rapidly scanning markers across the complete sets of DNA, or genomes, of many people to find genetic variations of disease - Single-nucleotide polymorphism (SNP): high-resolution markers in gene mapping related to diseases or normal traits - SNPs underlie differences in our susceptibility to a wide range of diseases - SNP is a single base pair difference in the DNA sequence of individual members of a species - SNPs are not all necessarily pathological, but are studied as a covarying marker of complex disease phenotype - Point mutation occurs when a single nucleotide is added, deleted, or substituted Psychiatric Disorders: COMT Gene: - Gene provides instructions for making an enzyme called catechol-O-methyltransferase (COMT) - Two versions of enzymes are made from COMT gene: Membrane-Bound COMT and Soluble COMT - In the brain (MB-COMT) helps break down neurotransmitters - Primary Function of MB-COMT: helps maintain appropriate levels of certain neurotransmitters in the brain = Dopamine, Epinephrine - Therefore, important to understand psychiatric disorders - Key enzyme for metabolism and inactivation of dopamine (excitatory) - Cytogenic Location: Long arm of chromosome 22 - Low activity of Val, Met alleles (result from COMP) results in slower inactivation of extracellular dopamine within the brain, especially in the prefrontal cortex - Anyone with this type of allele will have an abundance of dopamine

- Conclusion: the role of genetics in schizophrenia Brain Derived Neurotrophic Factor (BDNF) Gene: - Provides instructions for making a protein found in the brain and spinal cord called brain-derived neurotrophic factor - Promotes the survival of nerve cells - Promotes neuronal growth - Promotes maturation (differentiation of neurons) - Promotes maintenance of cell health - Involved in Synaptic Plasticity - Cytogenetic location: short arm of chromosome 11 - Regulates the survival and growth of neurons - Active at synapses, where communication occurs BDNF Serum Levels x Antidepressant Medication Status: - There is a decrease in BDNF levels in patients with persistent depression (relapse) - Relapse associated with higher levels of BDNF changes - Also true in bipolar disorder, in both mania and depressive phases - BDNF may represent a key factor in the pathogenesis of these psychiatric conditions - Study: Does medication impact BDNF levels? - BDNF levels highest for healthy controls, and lowest in depressed patients without medication - Medication can increase BDNF levels as a protective factor for depression Schizophrenia - Antipsychotic drugs are very potent and can often result in twitches and movement issues, however, schizophrenia is a very intense disease and these drugs offer relief from hallucinations - High genetic transmission with schizophrenia - Caused by an overactive dopamine system in the brain, flooding the prefrontal cortex - Increase in dopamine is related to low levels of GABA (inhibitory neurotransmitter) Schizophrenia: Immune Gene C4: - Component 4 (C4) gene can exist in multiple copies (from one to four) on each copy of chromosome 6 - Four different forms: C4A-short, C4B-short, C4A-long, C4B-long - C4 is an immune system Gene -- a small secreted protein that assists immune cells in the targeting and removal of pathogens - Schizophrenia: increased expressions of the C4 gene - C4A elevated expression levels is most strongly correlated with Schizophrenia

- Increased expression of C4A in cortical brian regions (prefrontal region) - C4A activity on cellular level: immune cells for the brain are microglia - In early brain maturation, C4 tags a synapse for pruning, the more C4 gets switched on, the more synapses get eliminated - Unusually variable across individuals, leading to distinct levels of immunity - Q: Is the brain overcleaning synapses that are useful in schizophrenia? Is there an overactivation of synaptic pruning? Is it misunderstanding synapses that are needed? - C4 gene is very important in supporting connections between neurons Microglia: - Act as the first and main form of active immune defense in the central nervous system - Are distributed in large non-overlapping regions throughout the CNS - Key cells in overall brain maintenance -- they are constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents - They respond to pathogens and injury by changing morphology and migrating to the site of infection/injury, where they destroy pathogens and remove damaged cells Is there increased synapse elimination by microglia in schizophrenia patients? - Brain scans show higher levels of microglia activity in people with schizophrenia - Synapse Engulfment, beyond synaptic pruning - Results in the abnormal development of high levels of synaptic pruning, over correction of synapses which depletes synapse which are healthy - Synapse engulfment directly impacts neuronal communication in schizophrenia - Specifically activated in adolescence and early adulthood - Coincides with when symptoms of schizophrenia first appear Bipolar Disorder: Dysregulated Dopamine System: - Extreme elevated mood - Decreased need for sleep - Flight of ideas - Restlessness - Grandiosity - Pressured, rapid speech - Over-activation at rest due to an overabundance of dopamine - Lithium is prescribed to treat bipolar disorder to reduce the excitation of sodium channels

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Normal Brain vs. PTSD - Shows overactivation of flight or fight response in PTSD patients - Causes amygdala to be overactive (emotion center), and lowers activation in prefrontal cortex (emotion regulation), shrinks hippocampus (glucocorticoid receptor sites) - Overactivation of a stress system Depression: Reduced activation in prefrontal region: - Involved in reasoning, judgement, emotion regulation - Role of inflammation: Those who are depressed for more than a decade have about 30% more brain inflammation - Inflammation leads to brain cell loss, the longer one is depressed the more there is a decrease in cognitive ability - Depression correlated with risk of developing alzheimer’s disease due to inflammation Serotonin, Tryptophan, and Depression: - Serotonin reuptake problem in depression - Serotonin is synthesized from the amino acid tryptophan - One of the main neurotransmitter candidates to be a mediator in regenerative processes in the CNS is serotonin - Tryptophan depletion is widely used paradigm to study serotonin in the pathophysiology and treatment of depression - Tryptophan depletion leads to brain cell loss - Depression may occur when there is a suppression of new brain cells, often caused by stress - Serotonin controls axon and neuronal regeneration Depression: - Depression is still considered a mood disorder and not a neural degeneration disorder - However depression increases inflammation in the brain when experienced for a long duration - However, regardless of the length of the depression, it is largely treated the same way with SSRIs - Treatment options for later treatment of depression may want to consider targeting inflammation in the brain - Inflammation will typically impact microglia

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- SUV: standardized uptake value (nuclear medicine term) - Represents the population average of plasma glucose concentrations (PET scans) - If a PET scan detects uptake, there might be a clinical relevance - Microglia are being measured/ too much inflammation that is associated with degenerative illnesses (ex. alzheimers) - When microglia are activated they make more translocator protein which are a marker of inflammation - Translocator protein levels were 30% higher in those with long duration of untreated depression - Shows a correlation between long duration of depression and risk of alzheimers

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Masculinities and Depression Overview of Depression: - Leading cause of disability worldwide - Only half of people with depression receive treatment - Effective therapy and medications - DSM diagnosis (symptoms not mechanisms) - Primary care physicians are most likely to be dealing with depression first The Depression Discrepancy - Epidemiological data is consist - Women are diagnosed with depression more than men - American College of Physicians: - Female sex is a risk factor → the conclusion made based of the data is that since more females are diagnosed with depression, the female sex is a risk factor for depression - Men die by suicide at 3-4 times the rate of women - Traditional, western masculinities associated with severity of depression - Also associated with less help-seeking - When “male-typical” symptoms accounted for, the discrepancy disappears - Substance use - Aggression - Risk taking - Not symptoms of depression according to DSM-5 Masculinities: - Gender justice - Focus on women/femininities - Critical masculinity studies became a necessary study - Hegemonic Masculinities: embodies the most honored way of being a man - Social - Fluid over time and space - Relational Help seeking and getting help: - An iterative, dynamic process that consists of various intra- and inter-personal steps, some of which are attitudinal, some are behavioral, and some are a combination - But also, just because you seek help doesn’t mean you will receive it

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Barriers: 1. Hegemonic masculinities shape experience and expression - Alexithymia → difficulty in communicating one’s emotions - Brownhill’s Big Build (2005)

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- However, the DSM is gender neutral… - Depression is a DSM diagnostic category - Only a category since 1980 - Majority of participants in experiments in the 50s - 70s were women - Before depression was even defined, it was already assumed to be a female ailment - Only a problem if men and women tend to present with depression differently - Martin et al. 2013 → when male typical symptoms used to diagnose, rates of diagnosis are same between men and women - Emphasizes the push to revise DSM definition - Leads to - People ignoring their own depression - Providers misdiagnosing 2. Heightening the stigma of depression - Experiences of depression can challenge core tenets of hegemonic masculinities - Control over emotions, toughness/self-reliance, work, etc. - Compared to women, men are - More reluctant to characterize themselves or other men as depressed - Express self-stigma - Hold a negative view of people with depression - Leads to hiding depression from self and others 3. Hegemonic masculinities pose barriers to seeking help - Conformity to hegemonic masculinities correlates with negative attitudes toward help-seeking (Addis et al.,2017) - Risky - Differences in help-seeking behavior between men and women disappear when endorsement of masculine norms is controlled for 4. Hegemonic masculinities further stigmatizes depression treatment - Different men have different preferences for therapy and medications - Many men stigmatize all forms of treatment to some degree - Counseling is too emotional - Medications take away your control - Belief that treatment doesn’t work - Won’t take risk of seeking help

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5. Hegemonic masculinities impede providers from recognizing depression in men - Providers less likely to diagnose men compared to women when they present with the same symptoms - Implicitly and explicitly trained Masculinities: creating barriers and facilitators: - Facilitators - therapy/medication can be seen as sources of control - Seeking help as responsible/proactive - Work - Family Gaps in the Research: - Mostly quantitative - Participants - White, college students, often don’t have depression (hypothetical) - Attitudinal > structural - Motivations rather than things like healthcare - Barriers > facilitators (less research) - Few interactions amongst barriers and facilitators - Before COVID - Things have changed Translational Neuroscience Definition: Translational neuroscience is the field of study which applies basic neuroscience research to translate or develop into clinical applications and novel therapies for nervous system disorders Translational Neuroscience: Neuroplasticity: - Functional plasticity: The brain’s ability to move functions from a damaged area of the brain to an undamaged area to carry out the functions - Structural plasticity: The brain’s ability to change its physical structure as a result of learning (alternate brain pathway) - Mechanism: Synaptic Pruning - Gives the knowledge to apply basic neuroscience knowledge of autism and synaptic pruning and schizophrenia and synaptic engulfment to translational neuroscience

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GABA (Inhibitory) Deficiency + Dopamine (Excitatory) Toxicity: - Schizophrenia: - Positive Symptoms: Hallucinations, delusions - Negative symptoms: Anhedonia, amotivation, social withdrawal, flat affect - Cognitive symptoms: poor short/long-term memory, speech/communication difficulties, inattention - Shows the connection to the neurochemical brain and how translational neuroscience has directly translated to antipsychotic medication Schizophrenia: Immune Gene C4: - Can use this knowledge to decide if you want to use CRISPR technology or not Social Anxiety Disorder: - Basic neuroscience informs translational neuroscience - Endorphins released in response to a 20 minute walk compared to sitting quietly - Why exercise is prescribed as treatment Deep Brain Stimulation: - “State of the art” translational neuroscience, very invasive - Involves implanting electrodes in targeted areas of the brain which deliver electrical signals that block or change the activity that causes symptoms - Currently approved to treat diseases that involve the motor circuit - Used in Parkinson’s to target the substantia nigra How did we get here? - DTI for DBS: - The complex interaction of DBS with the surrounding tissues must be scrutinized with DTI - Allows us to create hypotheses that can explain network interactions - Ensure that disruption does not cause harm to adjacent tissue - Have to understand the electrical brain → how will DBS affect other non-targeted areas of the brain - DTI allows us to understand these structural connections because of white-matter tracts

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Mindfulness Based Cognitive Therapy: - Encourages patients to become more aware of their thoughts, feelings, and bodily sensations - Encouraged to view thoughts as passing events in the mind - Effective in depression and anxiety - Removes the patient from negative thoughts and reduces risk of relapse fMRI: Large Scale Brain Networks: - Default mode network and alpha band coupling - Scientific basis that supports MBCT Neuromodulation (EEG): - Understanding of the electric brain - Focal brain stimulation: used to stimulate a neuron or neural network - Reweighting, reconnecting, rewiring, regenerating Transcranial Magnetic Stimulation: - Magnetic fields produce electrical currents that activate cells in the brain - Stimulates release of neurotransmitters - In depression, targets the left PFC Transcranial Direct Current Stimulation (tDCS) - Different from TMS: not stimulating a region but a pathway - Anode (excitatory) and Cathode (inhibitory) - Mechanism: electrical stimulation for hyper-perfusion (increased blood) of the brain - DC stimulation increases calcium and glial involvement that is global based - It will reprogram the brain - Induces a brain state of neuroplasticity - Combination of EEG and DTI makes this possible Left Hypo-Frontality in Depression: - Left-frontal region (positive emotions), right frontal (negative emotions) - Depressed people show less left hypo-frontal activity (F3 electrode region) - Frontal brain asymmetry in depression (more right frontal activation) associated with avoidance, negative emotion - Anhedonia: loss of pleasure, fatigue, low motivation - Consistent with self reporting of patients, shows withdrawal from positive experience rather than approach to negative

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Alpha Wave Levels & Disorders: - Left ALPHA hypo-frontality associated with mood disorders - Drug and alcohol addiction (left hyper-frontal alpha activity) - Synthetic relaxed state (not meditation) - Shows short term effects of TMR, high relapse rates EEG and Artificial Intelligence: Brain-Computer Interphase (BCI): - EEG and AI combined to both Neuromodulation and BCI Brain-Computer Interphase: - Technology that allows a human to control a computer, it then has an electric device to make the commands of the computer - Uses electrode to detect electrical signals in the brain and interprets brain signals that are sent to the computer - The computer translates electrical signals in the data to control the computer - Ex: exoskeleton - Wearable motor machine Translational Science: - Neurotransmitters and medication target: stabilizing the chemical brain - Neuromodulation: transcranial magnetic stimulation/ deep brain stimulation target: brain regions and circuit functioning - Optogenetics target: controlling neurons through laws of physics - Telomeres target: cellular aging - CRISPR: genome engineering - genome editing tool target: specific genes

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Post-Midterm Lecture Notes

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