disorder study guide

Major Depressive Disorder (MDD)

Characterized by periods of two or more weeks of a depressed state and anhedonia.

Anhedonia

The inability to gain pleasure from activities that are normally enjoyable.

Concordance rate for identical twins in MDD

About 50%.

Structural issues in MDD

Positive emotions are linked to left frontal lobe and depression in right frontal lobe.

Limbic irregularities in MDD

Increased activity in the amygdala and anterior cingulate cortex, and less activity in the prefrontal cortex.

Chemical issues in MDD

Elevated growth hormone, thyroid hormone, cortisol, glucocorticoids, lowered monoamines, HPA axis irregularities.

Sleep Irregularities in MDD

Fall asleep faster, enter REM earlier, less stime in stages 3 and 4, awaken frequently.

Monoamine theory of depression

Proposes that deficiencies in monoamines like serotonin, norepinephrine, and dopamine contribute to depression.

Issues with the monoamine theory

It minimizes other neurotransmitters' contributions such as glutamate and GABA.

Bipolar Disorder

Characterized by alternating periods of depression and manic states.

Concordance rate for bipolar disorder

Ranges from 70-90%.

Structural Issues with bipolar disorder

Basal ganglia function abnormalities and low grey matter in the prefrontal cortex and limbic structures.

Chemical issues in bipolar disorder

Involves an imbalance of monoamines, possibly too little serotonin and too much norepinephrine.

Positive symptoms of schizophrenia

Delusions, hallucinations, disorganized speech, and disorganized behavior.

Negative symptoms of schizophrenia

Social withdrawal and mood disturbances.

Genetic heritability in schizophrenia

Ranges from 40-60%.

Structural issues in schizophrenia

Tissue loss in the frontal cortex, anterior temporal lobes, and hypothalamus; enlarged ventricles; disorganized hippocampus cells.

Dopamine hypothesis of schizophrenia

Overabundance of dopamine may lead to hallucinations and delusions.

Anxiety disorders

A mutation in the SERT gene is linked to low serotonin and increased anxiety disorders.

CHR1 gene in anxiety disorders

Linked to corticotropin-releasing hormone which impacts the HPA axis which triggers cortisol release.

Panic disorder

Stimulants may initiate panic attacks by stimulating the locus coeruleus. Antidepressants may help.

OCD

Involves repetitive intrusive thoughts and ritualistic behaviors.

Concordance rate of OCD

68%

Structural issues in OCD

Abnormal activity in the basal ganglia, prefrontal cortex, orbitofrontal cortex, cingulate gyrus.

Alzheimer’s Disease

A progressive neurodegenerative disorder characterized by memory loss, impaired reasoning, language difficulties, and disorientation.

Structural problems in Alzheimer’s Disease

Includes shrinkage of the hippocampus, parietal lobes, and temporal lobes of up to 40%.

Baptist view on Alzheimer’s

Believes beta-amyloid plaques are harmful and linked to the disease.

Beta-amyloid plaques

Surrounded by degenerating axons and glial cells.

Taurist view on Alzheimer’s

Believes neurofibrillary tangles made of tau protein lead to Alzheimer's. Found in the hippocampus and cerebral cortex.

Main neurotransmitter linked to Alzheimer's

Acetylcholine which is synthesized by choline acetyltransferase by up to 90%.

Genes associated with early-onset Alzheimer’s

APP gene, presenilin genes, chromosomes 1, 14, and 21.

ApoE gene’s role in Alzheimer's

Linked to late-onset Alzheimer's, with increased risk associated with ApoE-4 allele.

Parkinson’s Disease symptoms

Difficulty moving, tremors, frozen facial expressions, stooped posture, dementia in later stages.

Structural problems in Parkinson’s Disease

Degeneration of substantia nigra and basal ganglia damage.

Dopamine levels in Parkinson’s Disease

Reduced to about 40% of normal levels.

Chemical issues in Parkinson’s Disease

Low levels of noradrenaline, serotonin, acetylcholine.

Genetic factor in early-onset Parkinson’s Disease

Alpha-synuclein gene mutation; guanine is changed to adenine.

Treatment options for Parkinson’s Disease

Stem cells and deep brain stimulation.

Huntington’s Disease

Produces involuntary jerky movements, depression, hallucinations, delusions.

Structural degeneration in Huntington’s Disease

General shrinkage of the brain by up to 20%, with significant striatum cell loss.

Chemical imbalances in Huntington’s Disease

Low GABA and acetylcholine levels, and high dopamine and glutamate levels.

Inheritance pattern of Huntington’s Disease

Autosomal dominant; 50% chance of passing to offspring.

Antidepressant categories

MAOIs, tricyclic antidepressants, and SSRIs.

Monoamine Oxidase Inhibitors

Can cause harmful side effects and dietary restrictions.

Tricyclic antidepressants

Inhibits reputake of serotonin and norepinephrine; acts on histamine and Ach.

Selective serotonin reuptake inhibitors (SSRIs)

Prozac, Zoloft, Lexapro; fewer side effects than tricyclics.

Evidence in favor of dopamine hypothesis

Drugs that block dopamine receptors lessen symptoms in schizophrenia.

Evidence against dopamine hypothesis

25% of patients do not respond to dopamine antagonists.

Revised dopamine hypothesis

Increase dopamine activity in mesolimbic areas and decrease dopamine activity in the prefrontal cortex.

Glutamate hypothesis for schizophrenia

Suggests glutamate levels may explain negative symptoms better than dopamine.

Treatment strategy for schizophrenia

Dopamine blockers, serotonin and dopamine blockers, TMS

Transmissible Spongiform Encephalopathies

Progressive neurodegenerative disorders characterized by cognitive, psychological, and motor disturbances.

Symptoms of TSE

Paranoia, anxiety, depression, cognition loss, motor disturbances, death

Scrapie

TSE in sheep

Bovine Spongiform Encephalopathy (BSE)

mad cow disease

Creutzfeldt-Jakob disease

TSE in humans

Kuru

TSE in humans

TSE infectious agents

Long incubation period, lack of inflammation, immunity to hospital sterilization

Prion characteristics

Abnormal proteins that cause TSEs due to misfolding.