Biological Explanations For Sz Flashcards
(15 cards)
What is meant by genetics
-genes consist of dna strands
-dna produces instructions for general physical characteristics of organism like eye colour and height but also specific physical features like neurotransmitter levels , size of brain structure
-may impact psychological features such as intelligence and mental disorder
Genes transmitted parents to offspring
How have family studies got a genetic basis in Sz
-confirmed risk of Sz incr in line with genetic similarity to a relative w disorder
-relationship is shown in graph which presents findings from irving gottesmans large scale family study
-as genetic similarity incr, so does probability of sharing Sz
-but identical twins not 100% as is 48% so environment must also have an impact (diathesis stress)
-9% if have sibling
-family members do tend to share aspects of their environment as well as genes, so correlation represents both
-family studies show importance of genes for Sz
How have candidate genes got a genetic basis in Sz
-early research in this area looked for a single genetic variation in belief one faulty gene could explain Sz
-but appears number of dif genes involved and each give a small increased risk
-Sz is polygenic
-one large study by Ripke et al combined all previous data form genome wide studies of Sz
-genetic makeup of 37000 people w Sz diagnosis compared to that of 113000 controls , 108 separate genetic variations associated with slightly increased risk of Sz
-bc diff studies have identified diff candidate genes, also appears Sz is aetiologically heterogenous , means diff combination of factors such as genetic variation can lead to the condition
What is the role of mutation in the genetic basis of Sz
-can also be caused by mutation, where there’s no family history of Sz
-mutation in parental dna caused by radiation, position, viral infection
-evidence for mutation comes from +ve correlations between paternal age (associated w increased risk of sperm mutation) + risk of Sz , incr from around 0.7% w father under 25 and over 2% in fathers over 50, found by brown et al
Whats a strength of the genetic explanation and its strong evidence base
Family studies such as gottesman show that risk increases with genetic similarity to family member w Sz
Adoption studies such as Tienari et al show biological children of parents w Sz are at heightened risk even if grow up in adoptive family
Recent twin study by Hilker et al showed a concordance rate of 33% for identical twins, and 7% for non-identical twins
Shows that some are more vulnerable to Sz as a result of their genetic makeup
Whats a limitation of the genetic explanation and that there’s clear evidence to show environmental factors also increase risk of developing Sz
Environmental factors include biological , psychological influences
Biological risk factors include birth complications , smoking THD-rich cannabis in teenage years
Psychological risk factors include childhood traumas , leaves people more vulnerable to adult mental health problems in general but there is now evidence for particular link w Sz
In Morkved study ,67% people w Sz + related psychotic disorders reported at least 1 childhood traumas as opposed to 38% of a matched group with non-psychotic mental health issues
Mean genetic factors alone cant provide a complete explanation for Sz
What is meant by neural correlates
-we don’t know what exactly causes Sz symptoms
-but research has identified some neural correlates
-these are measurements of stricter or function of brain activity that correlate with an experience
-it may be what causes an experience eg a positive symptom such as delusion
-dopamine (DA) best known neural correlate of Sz
What is dopamine
- a neurotransmitter than generally has excitatory effect , linked to sensation of pleasure, movements thinking, perception
-unusually high levels of-> sz
-unusually low levels -> parkinsons
How is the effects dopamine related to symptoms of sz
-feelings of pleasure - sz often accompanied by depression
-movement - less motivation
-thinking - delusions
-perception - Hallucinations
-incr in dopamine -> incr positive symptoms
-decr dopamine -> avolition - > incr -ve symptoms
Describe the original dopamine hypothesis (hyperdopaminerga)
-og hypothesis based on discovery that drugs used to treat Sz (antipsychotics, reduce DA) caused symptoms similar to those with Parkinson’s , condition w low DA levels
-sz may be result of high DA levels (hyperdopaminerga) in subcortical areas
Eg excess of DA receptors in pathways from sub cortex to Broca’s area (speech production) may explain specific symptoms of Sz like poverty of speech And auditory hallucinations
Describe the updated versions of the dopamine hypothesis (hypodopaminerga)
-Davis et al proposed cortical hypodopaminerga ie abnormally low DA in cortex
-this also explain Sz symptoms
-eg low DA in prefrontal (thinking area) could explain cognitive problems ie -ve symptoms of Sz
-also suggested cortical hypodopaminerga leads to subcortical hyperdopaminerga , so both high + low levels of DA in different brain regions are part of the updated version
-aswell as explaining links between abnormal DA levels + symptoms, current versions of dopamine hypothesis try explain origins of abnormal DA function
-seems both genetic variation + early experiences of stress (psychological / physical) make some ppl more sensitive to cortical hypodopaminerga , and so subcortical hyperdopaminerga
Whats a strength to support idea that DA is involved in Sz
first, amphetamines incr DA , worsen symptoms in people with Sz , + induce symptoms in people w out
second, antipsychotic drugs reduce DA activity + also reduce intensity of symptoms
third, some candidate genes act on production of DA or DA receptors
Strongly supports DA is involved in Sz symptoms
Whats a limitation of the dopamine hypothesis and evidence for a central role of glutamate
Post mortem + live scanning studies have consistently found raised levels of neurotransmitter glutamate in several brain regions of people w sz
In addition, several candidate genes for sz believed to be involved in glutamate production/processing
Means an equally strong case can be made for a role for other neurotransmitters
