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1
Q

What is the biochemical explanation of mental illness??

A

Electrical impulses travel around the brain.
Neurotransmitters pass across the synapse.
Symptoms of mental illness are due to abnormal neurotransmitter levels or action.

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2
Q

What is meant by the monoamine hypothesis?

A

A group of neurotransmitters that regulate mood.

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3
Q

Name three examples of monoamines

A

Serotonin
Noradrenaline
Dopamine

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4
Q

How do monoamines (in terms of low levels of serotonin) effect symptoms of depression?

A

Low levels of serotonin can cause levels of noradrenaline and dopamine to drop.
Low levels of noradrenaline linked to lack of pleasure.
Low levels of dopamine linked to anxiety.

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5
Q

What is the role of the gene 5-HTT?

A

Regulating serotonin levels
People with variations of 5-HTT gene that are under-active more likely to suffer depression after stressful life events.

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6
Q

What is the role of MAO-A?

A

Removes monoamines from the synapse.
If too much MAO-A removes monoamines leading to symptoms of depression.

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7
Q

Supporting evidence for the monoamine hypothesis

A

Meyer (2006)
17 participants with depression who hadn’t taken anti-depressants for 5 months.
17 ‘normal’ who were control group.
PET scans carried out.
Scans showed depressed patients had significantly higher MAOA levels in all brain areas tested.

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8
Q

What is meant by the genetic explanation of mental illness?

A

Characteristics are inherited from parents who pass on genes to us.

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9
Q

How are genetic principles investigated?

A

Concordance rates
Family studies
Twin studies
Adoption studies

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10
Q

Evidence for the role of genetics in relation to mental illness

A

Wender et al. (1986)- biological relatives of a depressed adoptee were x8 more likely than adoptive relatives to have depression.

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11
Q

What is the role of the serotonin transporter gene?

A

Gene responsible for producing serotonin which has been implicated in depression.
Short form of gene leads to inefficient serotonin production.

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12
Q

Supporting evidence of the serotonin transporter gene.

A

Ogilvie et al (1996)- Compared serotonin transported gene in39 people with major depression and 139 from general population.
Significantly higher occurrence of short alleles in depressed groups.

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13
Q

How are brain differences investigated?

A

PET scans- injected with glucose which emits positrons that can be detected by scanner.
MRI

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14
Q

What are the four brain areas implicated in depression?

A

Prefrontal cortex
Limbic system
Amygdala
Hippocampus

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15
Q

Evidence for the role of the brain in depression- Hippocampus

A

Repeated stress may cause neurones in hippocampus to shrink.
Depression may cause hippocampus to shrink/weaken.
Thompson et al (2015)- Study compared brain volume in people with or without depression.
- Depressed people had smaller hippocampus
- Brain differences became more severe the longer an individual suffers from depression.

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16
Q

Evidence for the role of the brain in depression- Prefrontal cortex

A

Shrink with depression.
Frodl- Researched brains of people with depression and compared them to people without depression.
-Abnormalities in hippocampus and prefrontal cortex
- Followed the depressed and non-depressed for three years, found continued decrease in these brain areas of people with depression.

17
Q

Evidence for the role of the brain in depression- Amygdala

A

Changes in activity in amygdala associated with symptoms of depression.
E.g. increase in activity found when depressed patients are presented with negative stimuli.
Sheline et al (2001)- fMRI scan on 11 depressed patients and 11 normal.
- Scans showed amygdala was more active in depressed patients when both resting and exposed to stimuli.