Biological Explanations Flashcards

1
Q

why is it difficult to untangle the genetic contributions to SZ

A
  • there is evidence that SZ runs in families. but families that share the same environment
  • strong relationship between the genetic similarity of family members and the likelihood of both developing SZ
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2
Q

is SZ an inherited disorder

A

people DO NOT inherit SZ
- but do inherit a genetic predisposition to it

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3
Q

Gottesmen 1991 carried out a family study and found the following concordance rates for SZ

A
  • MZ twin: 48%
  • DZ twins: 17%
  • Siblings: 9%
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4
Q

what do Gottesmen’s findings show

A

that the closer the degree of genetic relatedness, the greater the risk of developing SZ

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5
Q

what does it mean to say that SZ is polygenic

A
  • SZ might run in the family but no single gene is thought to be responsible.
  • polygenic meaning many genes are involved and a polygenic risk factor is calculated
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6
Q

what is the role of genetics in the aetiology of SZ

A
  • different combinations of these genes can lead to SZ.
  • therefore it is aetiologically (caused) heterogenous (by different things)
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7
Q

what were the findings of Ripke et al 2014

A

studied 37,000 patients and found 108 separate genetic variations associated with increased risk of SZ

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8
Q

why are adoption studies helpful in determining the aetiological role of genetics

A
  • a limitation with twin studies is that MZ twins have 100% same DNA they also share an environment
  • adoption studies allow for disentangling shared genes from the same environment
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9
Q

what were the findings of Tienari 2000

A
  • of the 164 adoptees whose biological mothers had SZ, 6.7% also were diagnosed compared to 2% of the 197 control group (no SZ mother)
  • this is support for a genetic explanation for SZ, but only that it increases the likelihood of developing SZ
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10
Q

what is the dopamine hypothesis of SZ

A
  • dopamine is a neurotransmitter
  • the original dopamine hypothesis stated that SZ was caused by excessive activity of dopamine in the subcortex
  • causes the neurons responding to dopamine fire too often and transmit too many messages
  • message ‘overload’ may produce many symptoms
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11
Q

what is hyperdopaminergia, in where is thought to occur in the brain in patients with SZ

A
  • high levels of dopamine in subcortical areas projecting to Broc’s area may be associated with the experience of auditory hallucinations and/or speech poverty
  • it is now thought people with SZ have high numbers of D2 receptors
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12
Q

what is an alternative explanation that would cause excessive dopaminergic activity

A

it may be that both hyperdopaminergia and hypodopaminergia are correct explanations - both high and low levels of dopamine in different brain regions are involved in SZ
- more recent version focuses on abnormal dompamine systems in the cortex

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13
Q

how does Goldman-Rakic’s 2004 work revise the dopamine hypothesis

A
  • identified low levels of dopamine in the prefrontal cortex in the negative symptoms of SZ such as avolition
  • the prefrontal cortex is responsible forthinking and decision making
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14
Q

what does the ‘neural correlates’ of something mean

A

refers to the measurements of the structure of function of the brain that correlate with an experience.
- both positive and negative symptoms have neural correlates

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15
Q

give an example of the neural correlates of SZ

A
  • proposes that SZ is caused by enlarged ventricles
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16
Q

describe how the stidy by Juckel et al 2006 on the neural correlates of negative symptoms

A
  • found negative correlation between ventral striatum activity and overall negative symptoms of SZ
  • loss of motivation may be explained by low level activity in this part of the brain
17
Q

describe the work by Allen et al. 2007 on the neural correlates of hallucinations

A
  • The superior temporal gyrus consists of the auditory cortex
  • found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus
18
Q

in what regard is research into the biological basis of SZ socially sensitive

A
  • thought to make patients appear less accountable for their disorders, which could increase clinician’s empathy
  • suggested that biological accounts of psychopathology can exacerbate perceptions of patients as abnormal, distinct from the rest of the population, meriting social exclusion, and even less than fully human
    -ongoing shift toward biomedical conceptualisations has many benefits, Lebowitz et al’s (2014) results reveal unintended negative consequences.
19
Q

how might a biological explanation of SZ be seen as reductionist

A
  • the effective use of drug treatment increases support for biological explanations of SZ
20
Q

PEEL - A problem with the genetic argument is that it is difficult to separate the impact of nature and nurture

A

p - difficult to separate the impact of nature and nurture
e - both family and twin studies investigate individuals who are sharing the same environment, which could be increasing the concordance rates, irrespective of the genes
e - high concordance rates between MZ twins is actually due to them being treated more similarly than DZ twins or ordinary siblings and not in fact due to their genetics
l - could be a confounding variable

21
Q

PEEL - a strength with the genetic argument is that there is very strong evidence from multiple sources

A

p - strong evidence from multiple sources
e - Gottesman (1991) Tienari et al (2004)
e - overwhelming evidence to support that genetics makes people more susceptible to developing SZ
l - It may be that genetics are not the only factor in the development of SZ but it does suggest a genetic vulnerability

22
Q

PEEL - A limitation with the dopamine hypothesis explanation of sz is there is mixed evidence

A

p - there is mixed evidence
e - amphetamines increase levels of dopamine and can make sz worse & antipsychotic drugs reduce levels of dopamine and can reduce symptoms in sufferers. BUT Ripke suggests other significant neurotransmitters other than dopamine that play a role
e - research has shifted and is investigating the role of the neurotransmitter glutamate
l - does not offer a complete explanation

23
Q

PEEL - what are limitations of studies in which the neural correlates of symptoms are identified

A

p - results are only correlational
e - may be that lower ventral striatum activity may cause negative symptoms of SZ such as avolition
e - difficult to use this correlational evidence to imply causation because there may be other intervening factors such as the environment that causes this effect
l - neural correlates is valid argument