week 13 lecture 20 mood and depression

Neurological Diseases features

Damage to once healthy tissue, progressive, lead to death, sometimes be pin-pointed to one structure in brain

Affective Disorders features

not progressive, Neural tissue not damage, Changes from wiring and circuit maturation

Affective Disorders principle

There is not a one-to-one relationship between structure and function when defining biological basis of emotion. It is a highly complex, integrated system that is not well understood

Affective disorders factors

genetic, NTs, complex emotions, environmental

affective disorder definiton

mental disorder with dramatic changes or extremes of mood

what kind of episodes could affective disorder have

manic, depressive

manic episodes features

elevated, expansive, or irritable mood with hyperactivity, pressured speech, inflated self-esteem

depressive episodes features

dejected mood with disinterest in life, sleep disturbance, agitation, feelings of worthlessness or guilt or combo

what type of symptom could affective disorder have

psychotic

psychotic symptoms

delusions, hallucinations, other loss of contact with reality

how to know someone might have Affective Disorder

experiences fluctuations in mood, cause significant impairment because feelings are so extreme, Symptoms must persist throughout a period of time

major types of depression

major, persistent

Major Depression features

Interferes with daily life, severe symptoms, Interfere with ability to work, sleep, study, eat, and enjoy life, episode can occur only once in a lifetime or has several episodes

Persistent Depressive Disorder features

Depressed mood that lasts for at least 2 years, may have episodes of major depression along with periods of less severe symptoms, but symptoms must last for 2 years

Major depression symptoms

Depressed mood, Diminished interest or pleasure, Change in weight, Change in sleep pattern, Psychomotor agitation or retardation, Loss of energy, Feelings of worthlessness or excessive guilt, Trouble concentrating, Recurrent thoughts of death and dying

major depression diagnostic questions

5 or more symptoms over a 2 week period, Symptoms cause clinically significant distress or impairment in social, occupational or other important areas of functioning, Symptoms not due to substance use or general medical condition, occurrence is not better explained by an unspecified schizophrenia or other psychotic disorder, has never been a manic episode or hypomanic episode

different types of depression

psychotic, postpartum, seasonal affective disorder

Psychotic depression

Severe depression plus some form of psychosis (delusions or hallucinations)

Postpartum depression

Hormonal and physical changes coupled with the responsibility of caring for a newborn

Postpartum depression stats

10-15% of women suffer after giving birth

Seasonal Affective disorder (SAD)

Onset during winter months when less natural sunlight

Seasonal Affective disorder (SAD) treatments

blue light and antidepressant medication

retinal ganglion cells involved with Seasonal Affective disorder (SAD)

Melanopsin

what defines the 4 connectivitiy-based biotypes of depression

canonical correlation analysis (CCA) and hierarchical clustering

how do areas of the brain show major depression

decrease in volume and extreme activity

Major Depression causes

Circuit Dysfunction, Neuroinflammation, Neuroplasticity hypothesis, genetic, polygenetic

what hypothesis is associated with Circuit Dysfunction

Monoamine hypothesis: Serotonin, dopamine, norepinephrine, epinephrine

what is the Monoamine hypothesis

Decrease in catecholamines leads to depression, Increase in catecholamines leads to manic episodes, But it is not in only one circuit

what system affects the prefrontal circuit of the Monoamine hypothesis

limbic system

what structure affects the hippocampal axis of the Monoamine hypothesis

amygdala

what structure affects the motivational circuits of the Monoamine hypothesis

nucleus accumbens

how is neuroinflammation a major depression cause

microglial activation

what is the neuroplasticity hypothesis

BDNF decreases in depression, but is elevated with antidepressants, Ketamine boots synaptogenesis (dendritic spines)

how is genetic a major depression cause

polymorphism repeats, People with both alleles that are long are less likely to become depressed, while people with one short and one long or two short alleles are more likely to develop depression

how is polygenetic a major depression cause

there isn’t one gene involved, 100+ variants

major depression treatments

Monoamine Oxidase Inhibitors, Selective Serotonin Reuptake Inhibitors, Ketamine/Esketamine, Psychedelic-Assisted Therapy

Monoamine Oxidase Inhibitors (MAOIs)

MO enzymes destroy dopamine, serotonin, norepinephrine in cytosol

what is Selective Serotonin Reuptake Inhibitors (SSRI) used for

treatment of depression, anxiety, OCD

Ketamine/Esketamine (Spravato)

Approved for treatment-resistant depression, NMDA receptor antagonist, Boosts BDNF, synaptic plasticity

Psychedelic-Assisted Therapy (Psilocybin)

Two pivotal Phase 3 trials completed, strong contender for FDA approval

Psychedelic-Assisted Therapy (Psilocybin) mechanism

5-HT2A agonism → neuroplasticity + emotional processing shifts

what do they do When antidepressant treatments fail

Deep Brain Stimulation

Treatment-resistant Depression

DBS

what do they do in Deep Brain Stimulation

Bilateral electrodes placed in subgenual cingulate region, stimulates white matter tracts

what happens with the activity of BA 25 in people with bipolar disorder

increases during a manic episode and decreases during the depressive phase

what is FDA-approved for treatment-resistant depression and works by modulating prefrontal–limbic circuits

Repetitive transcranial magnetic stimulation (rTMS)

where are bilateral electrodes placed in with Deep Brain Stimulation

Brodmann area 25