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Molecular Principles of Brain Disorders > Depression > Flashcards

Depression Flashcards

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1
Q

what is the Monoamine Hypothesis?

A

predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin (norepinephrine, dopamine) in the central nervous system

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2
Q

what is a lifestyle disease?

Is depression a lifestyle disease?

A

Lifestyle diseases are diseases that appear to increase in frequency as countries become more industrialised and people live longer

no, depression is not a lifestyle disease

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3
Q

What are the current etiology ideas regarding depression?

A
  1. overactive Amygdala
  2. overactive HPA-axis
  3. decreased PFC (pre-frontal cortex)
  4. decreased hippocampal volume
  5. decreased levels BDNF

Depression characterised by increased and sustained emotional reactivity

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4
Q

What are symptoms of depression

A

depressed mood, decreased motivation/interest, significant weight loss/gain, insomnia/hypersomnia, feelings of worthlessness, recurrent thought of death/suicide

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5
Q

what factors dominate the occurrence of depression

A
  1. unemployment
  2. disability
  3. suicide attempts
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6
Q

why is depression diagnosis difficult?

A

Lack of objective diagnostic tests > depression is a compilation of symptoms
–> it is based on verbal information ( biomarkers would be useful)

(thin line between mild depression and neurotypical sadness)
No clear line distinguishing people with mild clinical depression from
those having tough time in course of normal life

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7
Q

Explain brain-imaging findings on Increased Amygdala reactivity

A

Amygdala = processing of emotions and memories associated with fear.

  1. Increased and sustained amygdala reactivity especially in response to emotional information

(positive, neutral and negative information provide increased amygdala activity in depressed patients compared to neurotypical patients)

  1. involuntary elaboration on negative topics, higher amygdala activity than the others (+ en -)
  2. SSRI’s research: decrease amygdala activity, patient feels better.

treatment = Pharmacotherapy and behavioral therapy can normalize amygdala and
PFC functioning

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8
Q

Explain brain-imaging findings on Decreased PFC activity

A

PFC = central role in cognitive control functions, and dopamine in the PFC modulates cognitive control, thereby influencing attention, impulse inhibition, prospective memory, and cognitive flexibility.

  1. decreased PFC activity in response to cognitive tasks (digit-sorting tasks), but no performance deficits
  2. interaction PFC and amygdala: insufficient for brain circuit inhibition.

treatment = Pharmacotherapy and behavioral therapy can normalize amygdala and
PFC functioning

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9
Q

Explain the contradictory results on reduced hippocampal volume in studies

A
  1. dependent on the subtype of depression
  2. reduced hippocampal volume when depressed/ normal volume when treated/non-depressed
  3. indicator for vulnerability of depression in healthy people
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10
Q

How could Reduced Hippocampal volume occur

A
  1. loss of volume neurons : dendritic atrophy and spine loss; decreased neuronal synapses
  2. loss of number neurons : inhibition neurogenesis (only in hippocampus)
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11
Q

What is the role of the HPA-axis in depression?

A

overactive HPA-axis present in subtypes of depression

  1. increased cortisol
  2. increased CRH
  3. reduced GR’s
  4. anxiety, weight loss, chronic stress

attributes to the “grey glasses” of depression

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12
Q

how can HPA-axis be restored in depression

A

Most AD and psychotherapy (and possibly other treatments) can restore efficient negative feedback by increasing gene/protein expression of GC-R in hypothalamus and hippocampus

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13
Q

what is BDNF

A

Brain Derived Neurotrophic factor

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14
Q

What is the role of BDNF in depression

A

BDNF levels in adult brain: neuronal survival, synaptic plasticity, synaptogenesis, dendrites, neurogenesis

depressed patients show low levels of BDNF –> contribute to the hippocampal volume loss

antidepressants increase BDNF expression

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15
Q

How are the HPA-axis and BDNF levels connected

A

high cortisol levels lead to low BDNF levels

  1. high cortisol
  2. cortisol binds to GR’s
  3. Transcription factor translocates to nucleus
  4. lowers expression of BDNF
  5. less neurogenesis
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16
Q

How are HPA-axis and Hippocampal volume connected

A

High cortisol levels lead to reduced hippocampal volume

  1. high cortisol
  2. atrophy dendrites
  3. BDNF decrease
  4. less neurogenesis
17
Q

Explain the Brain-gut hypothesis

A
  • In the gut also neurons and neurotransmitters are present ‘gut brain’
  • The ‘gut brain’ is also connected to the brain in a bidirectional way
  • The quality of the microbiome is found to be increasingly important for health in whole body and brain: paradigm shift
  • Your brain-gut connections and your gut microbiome can influence probability of brain disorders!

treatment = effects of food, antibiotics, probiotics on mood

18
Q

what are cytokines

A

pro-inflammatory mediators of the immune system

19
Q

name some cytokine biomarkers

A

IL-6, IL-1, TNF-a

20
Q

Define the cytokine hypotheses

A

secretion and production of cytokines increase the subset of depression

hypothesis: cytokines can modulate mood.

there is a high similarity between sick behaviour and depressed behaviour.
–> withdrawal from environment and pain/decreased reactivity.

21
Q

Connect the cytokine and chronobiological models

A

mice kept in the dark for a month displayed increased levels of IL-6

  1. Depression-like behaviour
  2. altered gene expression in HC for genes per2 and npas2
22
Q

What is the underlying mechanism of Ketamine

A

NMDA-antagonist

  1. induces synaptogenesis
  2. reversal of atrophy
23
Q

Psilocybin research possible treatment for depression?

A

Psilocybin therapy is an approach being investigated for the treatment of mental health challenges. It combines the pharmacological effects of psilocybin, a psychoactive substance, with psychological support. Psilocybin is an active ingredient in some species of mushrooms, often referred to as ‘magic mushrooms’.

24
Q

What is the circadian rhythm disruption? how does this inspire a new antidepressant

A

circadian rhythm disruption can cause depression.

treatment with light therapy can serve as anti-depressant
–> agomelatine: synthetic melatonin receptor agonist + serotonin 2C receptor antagonist

blue light therapy shown to induce more happiness

25
Q

what is the heritability of depression

A

mild: 25%
moderate: 40-50%
severe (BD): 80%

26
Q

Name gene-environment interactions in depression (5-HTT)

A

the 5-HTT (serotonin transporter) gene.

s: short –> low affinity
ll: long –> high affinity

based on genotype you have an increased link for depression with 5-HTT ss.

27
Q

Name gene-gene-environment interactions in depression (val/met or s/s)

A

Maltreatment is a severe form of life-event

val/met with s/s variant of BDNF show to create an 26% increased risk for depression

Molecular Principles of Brain Disorders (15 decks)

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