Biological explanations for Schizophrenia Flashcards
what have family studies found?
that the risk of schizophrenia increases in line with genetic similarity to a relative with the disorder.
e.g. findings from Gottesman’s large-scale family study.
e.g. someone with an aunt with schizophrenia has 2% chance of developing it, increasing to 9% if the individual is a sibling and 48% is they are an identical twin
family members also tend to share aspects of their environment as well as many of their genes - so correlation represents both
but family studies have good support for the importance of genes in schizophrenia
candidate genes :
early research looked for a single genetic variation in the belief that one faulty gene could explain schizophrenia.
but it appears there are a number of genes involves
schizophrenia is polygenic
the most likely genes would be those coding for neurotransmitters including dopamine
candidate genes - study RIPKE
Ripke combined all previous data from genome-wide studies (those looking at the whole human genome instead of particular genes) of schizophrenia.
the genetic makeup of 37,000 people with a diagnosis of schizophrenia was compared to that of 113,000 controls, 108 separate genetic variations were associated with slightly increased risk of schizophrenia
because different studies identified different candidate genes, it appears that schizophrenia is aetiologically heterogeneous
(different combos of factors - including genetic variation, can lead to the condition)
DRD2 gene codes for DA synthesising, GABA and Glutamate
what is the role of mutation in schizophrenia?
it can have a genetic origin in the absence of family history of the disorder
one explanation for this is mutation in parental DNA which can be caused by radiation, poison or viral infection
where does the evidence for mutation come from?
evidence for mutation comes from positive correlations between paternal age -
associated with increased risk of sperm mutation, and risk of schizophrenia increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al.)
what are the neural correlates that research has identified?
research has identified some neural correlates i.e. brain structure or function
an example of this is the neurotransmitter dopamine - which is importnant in the functioning of several brain systems related to the symptoms of schizophrenia
what was the original hypothesis of dopamine ?
it was based on the discovery that drugs used to treat schizophrenia (antipsychotics that reduce dopamine) caused symptoms similar to those in people with Parkinson’s disease - a condition associated with low dopamine levels
so schizophrenia may be the result of high levels of dopamine (hyperdopaminergic) in subcortical areas of the brain
e.g. excess dopamine receptors in pathways from the subcortex to Broca’s area - may explain specific symptoms of schizophrenia such as poverty of speech/ and or auditory hallucinations
what is the updated dopamine hypothesis?
Davis proposed the addition of cortical hypodopaminergia (abnormally low DA in the brain’s cortex)
this can also explain symptoms of schizophrenia
e.g. low DA in the prefrontal cortex could explain cognitive problems such as negative symptoms of schizophrenia
It was has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia - so both high and low levels of DA in different brain regions are part of the updated version.
the current version of the dopamine hypothesis try to explain the origins of abnormal DA function - so it seems that both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopinergia and so subcortical hyperdopaminergia
Strength - research support of genetic explanation : strong evidence base
Gottesman’s family study shows that risk increases with genetic similarity to a family member with schizophrenia
adoption studies such as Tienari show that biological children of parents with schizophrenia are at heightened risk even if they grow ip in an adoptive family
recent study by Hilker showed a concordance rate of 33% for identical twins and 7% for non-identical twins
shows that some people are more vulnerable to schizophrenia as a result of their genetic make-up
Limitation of genetic explanation - clear evidence to show that environmental factors also increase the risk of developing schizophrenia:
environmental factors include both biological and psychological factors
biological risk factors = birth complications (Morgan) and smoking THC-rich cannabis in teenage years (Di-Forti).
Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is evidence for a particular link with schizophrenia
study by Morkved - 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma opposed to 38% of a matched group with non-psychotic mental health issues
means that genetic factors alone cannot provide a complete explanation for schizophrenia
extra - genetic counselling
application of our understanding of the likely role of genes in schizophrenia is genetic counselling
if one or more potential parents have a relative with schizophrenia, they risk having a child who would go on to develop the condition
but the risk estimate provided by genetic counselling is just an average figure - it will not really reflect the probability of a particular child going on to develop schizophrenia because they will experience a particular environment which also has risk factors
Strength - evidence for dopamine
Strength is support for the idea that dopamine is involved in schizophrenia
amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without (Durran)
And antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher)
Also, some candidate genes act on the production of DA or DA receptors.
this strongly suggests that dopamine is involved in the symptoms of schizophrenia
Glutamate - Limitation
Limitation of the dopamine hypothesis is evidence for central role of glutamate
Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon)
Also, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing
this means that an equally strong case can be made for a role for other neurotransmitters
extra - Amphetamine psychosis
Tenn induced schizophrenia like symptoms in rats using amphetamines and the relieved symptoms using drugs that reduce DA action - this supports the dopamine hypothesis
But other drugs also increase DA levels (apomorphine) do not cause schizophrenia like symptoms (Depatie and Lai)
Garson has challenged the idea that amphetamine psychosis closely mimics schizophrenia
example of a gene mutation in rats
Grin2a mutation -affecting dopamine and glutamate
