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Schizophrenia - Biological explanations - Coggle Diagram
Schizophrenia - Biological explanations
Genetic basis
Gottesman's
family studies confirm risk increases with genetic similarity to a relative w/ schizophrenia
Schizophrenic aunt = 2% chance to develope (compared to normal 1%)
Sibling = 9%
Monozygotic twin = 48%
Cannot isolate the effects of genetics as family share aspects of environment aswell, so correlation represents both, but still support importance of genetics in likelihood to develope schizophrenia
Candidate genes - Polygenic (affected by multiople genes), those coding for regulation of neurotransmitters including dopamine
Ripke et al. compared the genetic make-up of 37,000 people diagnosed with schizo to 113,000 controls and found 108 genetic variations associated w increased risk
Mutations
, mutation in parental gametes caused by radiation, poison or viral infection
Brown et al.
evidence shown in positive correlation between paternal age, increasing risk of sperm mutation, and risk of schizophrenia
fathers under 25 = 0.7%
fathers over 50 = < 2%
Neural
best understood neural correlation of schizophrenia is variations in functioning of dopamine - important for functioning of several neural systems related to the symptoms
Dopamine Hypothosis
Davis et al.
- cortial hypodopaminergia (low) cause cognitive problems (due to impaired function of prefrontal cortex) leading to negative symptoms, this can cause subcortial hyperdopaminergia
Seeman
- subortial hyperdopaminergia (high) causes excess dopamine receptos in pathways connecting subcortex to Broca's area (responsibel for speech production) cause speech poverty and auditory hallucinations
There are both high and low dopamine levels in different brain regions
Howes et al.
genetic variations and early high stress experiences, both phsychological and physical, increase sensitivity to cortial hypodopaminergia and therfore also subcortical hyperdopaminergia concerquently
Patel,
investigated dopamine levels in schizophrenic and normal individuals using PET scans and found lower dopamine levels in prefrontal cortex
aetiologically heterogenous
, different combinations of factors including genetic variation can lead to schizophrenia
Evaluation
Supporting
The dopamine hypothoseis is suppoted by
Amphetamines
worsoning schizo syntoms in people w/ the disorder and inducing them in some individuals without it (
Curran et al.
)
Some candidate genes also act on production of dopamine and it's receptors
Tenn et al.
induced schizo symptoms in rats using amphetamines and relived symptoms using Dopamine action supressing drugs
Limitations
proof of the genetic basis is shown by family studies, however common rearing patterns within families may be the main cause of this, and not be very hereditary
For example, a negative emotional climate that leads to stress beyond an individuals ability to cope can trigger a schizophrenic episode
However,
Tienari et al.
adoption studies show children who's biological parents are schizophrenic are at heightened risk even if raised in an adoptive family
A twin study conducted by
Hilker et al.
showed 33% concordance in monozygotic twins and onlly 7% for dizygotic twins
Environmental factors
are also significant
Biological risk factors,
birth complication (
Morgan et al.
), and smoking THC-rich cannabis during teenage years (Di Forti et al.)
Psychological risk factors,
childhood trauma (
Mokved et al.
found 67% of peope with schizo reported child trauma, opposed to 38% of those with a non-psychotic mental disorder)