Biological explanations Flashcards

1
Q

What are genetics?

Genetic basis

A
  • Genes consist of DNA, which provides instructions for general physical features of an organism
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2
Q

What does family studies research show a connection between?

Genetic basis

A
  • Genetics (DNA) and environment
    (nature vs nurture)
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3
Q

What did Gottesman’s family studies research find?

Genetic basis

A
  • 48% of Mz twins share schizophrenia
  • 17% Dz twins
  • 9% siblings
  • 6% with parents
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4
Q

What are candidate genes?

Genetic basis

A
  • Genes that increase vulnerability of developing a disorder
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5
Q

What does schizophrenia being polygenic mean?

Genetic basis

A
  • There are a number of different genes involved
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6
Q

What did Ripke find about genes and schizophrenia?

Genetic basis

A
  • Combined previous genome-wide study of schizophrenia data
  • Genetic make-up of 37,000 people with schizophrenia vs 113,000 without
  • Found 108 separate candidate genes
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7
Q

What is an example of candidate genes in schizophrenia?

Genetic basis

A
  • Candidate genes code for DRD2
  • DRD2 codes for GABA, glutamate, DA synthesising
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8
Q

What is meant by schizophrenia being aetiologically heterogeneous?

Genetic basis

A
  • Different combinations of (genetic) factors can lead to the disorder
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9
Q

What is the role of mutation in schizophrenia?

Genetic basis

A
  • Mutation in parent DNA may be caused by: radiation, poison, viral infection
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10
Q

What did Brown find about mutation?

Genetic basis

A
  • Positive correlation between paternal age (increased risk of sperm mutation) and risk of schizophrenia
  • Risk increases from 0.7% with fathers under 25, to 2% in fathers 50+
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11
Q

Strength-
I- Research support

Genetic basis

A

D- Tienari found that adoption studies show that biological children of schizophrenic parents are at heightened risk, even in they grow up adopted. Hilker found concordance rates of 33% for MZ twins, and 7% for DZ twins
E- Shows that some people are more vulnerable due to genetic factors

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12
Q

Limitation-
I- Environmental risk factors

Genetic basis

A

D- Biological risk factors include birth complications (Morgan) and smoking THC-rich cannabis in teen years (Di Forti). Psychological risk factors include childhood trauma (vulnerability to adult mental health problems). Morkved found 67% of people with schizophrenia/ psychotic-related disorders reporpted at least one childhood trauma vs 38% matched group (alternative mental health issues)
E- Means genetic risk factors alone cannot provide a complete explanation

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13
Q

Evaluation extra-
I- Genetic counselling

Genetic basis

A

D- Practical application as parents are aware of schizophrenia in the family, their child is at higher risk, so genetic counselling informs potential parents of these probabilities so they can make informed choices about whether to have children who may have poorer quality lives. However, the risk estimate is an average, so does not reflect probability of individual children
E- Means it only provides a crude estimate of the risk of an unborn child developing schizophrenia

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14
Q

What is the original dopamine hypothesis?

Neural basis

A
  • Seeman= drugs used to treat schizophrenia (antipsychotics- reduce DA) cause symptoms similar to those with Parkinson’s (low DA)
  • So schizophrenia may be the result of high DA levels (hyperdopaminergia) in subcortical areas of the brain. For example, an excess of DA receptors in pathways from subcortex to Broca’s area may explain certain symptoms (speech poverty, auditory hallucinations)
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15
Q

What are neural correlates?

A
  • Patterns of structure/activity in the brain that occur in conjunction with an experience, and may be implicated in the origins of that experience

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16
Q

What is hyperdopaminergia?

Neural basis

A
  • Abnormally high levels of dopamine in the brain’s cortex
17
Q

What is hypodopaminergia?

Neural basis

A
  • Abnormally low levels of dopamine in the brain’s cortex
18
Q

What did Davis find about the dopamine hypothesis?

Neural basis

A
  • Proposed the addition of cortical hypodopaminergia, which explains symptoms (i.e. low DA in prefrontal cortex explains cognitive problems- negative symptoms)
19
Q

What is the role of hypodopaminergia in the updated dopamine hypothesis?

Neural basis

A
  • Cortical hypodopaminergia leads to subcortical hyperdopaminergia= both high and low levels of DA in different regions
20
Q

What does the updated dopamine hypothesis tell us about the origins of DA function?

Neural basis

A
  • It appears that genetic variations and early experiences of stress (physical/psychological) make some people more senisitve to cortical hypodopaminergia and subcortical hyperdopaminergia (Howe)
21
Q

Strength-
I- Evidence for the role of dopamine

Neural basis

A

D- Curran found that amphetamines increase DA and worsen symptoms in schizophrenic people, and induce symptoms in those without. Tauscher found antipscyhotic drugs reduce DA activity and reduce symptom intensity. Some candidate genes act on DA production/DA receptors
E- Suggests that DA is involved in symptoms

22
Q

Limitation-
I- Evidence for the role of glutamate

Neural basis

A

D- McCutcheon- post mortem and live scanning studies consistently found raised levels of glutamate in several brain regions in people with schizophrenia. Several candidate genes are believed to be involved in glutamate production/processing
E- Means an equally strong case can be made for glutamate

23
Q

Evaluation extra-
I- Amphetamine psychosis

Neural basis

A

D- Amphetamines (i.e. speed) can reproduce schizophrenia symptoms. Tenn induced symptoms in rats using amphetamines and relieved symptoms using drugs that reduce DA action. However, other drugs, such as apomorphine that increase DA levels do not cause symptoms (Depatie and Lal). Garson challenged Tenn’s idea. Animal studies also have poor generalisability
E- Research supports the link between amphetamines and symptoms, but evidence is not strong enough to support the DA hypothesis