biological expl Flashcards
candidate genes
-its a gene that could cause a disorder
-early research aimed to find 1 specific gene
-now its believed to be ‘polygenic’
-different researcg has suggested different genes to be involved, so we believe that sz is aetiologically heterogeneous
CG
polygenic
-mulitple genes involved, most of which r linked to coding for neurotransmitters
cg
Aetiologically heterogeneous
A number of different combinations of genes can lead to the illness
family studies
-family members share some of the same genes
-so we can investigate chanves of inheriting sz by looking at occurence of symptoms in family numbers
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families studies
gottesmans 1991
-large scale family study
-found if family member has sz the concordance rates are:
* Identical twins/mz: 48%
* Non-identical twins/dz: 17%
* Children: 13%
* Siblings: 9%
* Parents: 6%
* Half-siblings: 6%
* Grandchildren: 5%
* Nephews/nieces: 4%
* Uncles/aunts: 2%
* First cousins: 2%
* General population: 1%**
The Dopamine Hypothesis
Hyperdopaminergia
-higher than usual levels of dopamine in subcortex
-linked w positive symptoms such as hallucinations
-may be high number of dopamine receptors causing over activity of dopamine=cause sensory hallucinations
The Dopamine Hypothesis
Hypodopamineriga
-refers to lower than usual levels of dopamine in cortex
-where less dopamine is being transmitted across synpases
-linked w negative symptoms as theres a reducing in normal functioning
neural correlates
-more evidence that sz is down to abnormalities in brain
-structure of functioning of brain is associated w positive+negative symptoms
neural correlates:
negative symptoms
-ventral striatum is involved w reward anticipation
-sz ppts found to have less activty in this region-lower the activity the ^ severe the sympyoms
=explains avoloition
neural correlates:
positive symptoms
-allen at al (2007): scanned brains of ppts w hallucin ations whilst they completed an audiotry processing task
-lower activation levels=found in superior temporal gyrus+anterior cingulate gyrus
-they made more errors compared to control group
-auditory hallucinations= therefore correlated w reduced activity in these areas
role of mutation
-sz also have gentic orgin in absence of family history of the disorder
-one expl is mutation in parentakl dna which can be caused by radiation,poison or viral infection
-evidence comes from positives correlations between paternal age (^risk of sperm mutation)+risk of SZ ^ from around 0.7% w dads under 25 to over 2% in fathers over 50 (brown et al 2002)
AO3 –
flaw to twin studies
-assumption enviroment between DZ+MZ twins=the same
-joseph et al=MZ twins=^likely to be treated the same so explain ^ concordance rates as enviroment (nurture) rather than genes alone (nature) play part
-concordance rates not 100%-genes dont fully explian so could be diathesis stress model= reductionist+not considered othr factors eg biochem
-also DZ treated more like indivuals which expls low CR so diff in enviroment=nurture=big factor
-the shared enviroment=confounding variable
ao3
families studies research support
-gottesmans (1991) genetic similarity ^ risk of disorder
-tienari(2004) demonstrate gow kids who were adopted but had sz parents still at higher risk of sz
-molecular level research: ripke 2014= show particular genetic variations ^ risk of sz
ao3
dopamine support
-comes from success of drug trails that work to reduce affects of dop on brain
-antipsychotic drugs reduce effects of it+also symptoms of sz
-leucht et al (2013) carried out meta analysis of 212 studies that compared AP meds to placebos.
-results found AP were significantly ^ effective than placebos in treating pos+neg symps of sz
ao3 counterpoint to dop support
-ap drugs look to reduce dop+so symps of disorder, drugs that ^ dop should also ^ symps if dop hypothesius has validity
-this is exactly whats found w drugs such as amphetamines which ^ dop in brain (curran et al 2004)+thus symps of disorder supporting dop hypothesis
