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Biological Explanation Book Notes - Coggle Diagram
Biological Explanation Book Notes
Genetic Basis
Schizophrenia runs in families. This is quite weak evidence in itself for a genetic link because family members tend to share aspects of their environment. Therefore, sometimes it can be hard to dingusist between whether the cause is more due to genetics or environmental factors.
We share 100% of our genes with an identical twin and 50% with a sibling or parents. Thus, there is a strong relationship between the degree of genetic similarity and the shared risk of schizophrenia.
Candidate genes
It appear that schizophrenia is polygenic.
It also appears that schizophrenia is aetiologically heterogeneous.
Stephen Ripke et al 2004
He carried out a huge study combining all previous data from genome wide studies of schizophrenia.
The genetic make up of 37,000 patients were to compared to over 100,000 controls.
He found…
That there were over 100 separate genetic variations that were associated with increased risk of schizophrenia.
Genes associated with increased risk included those coidng for the functioning f a number of neurotransmitters including dopamine.
Clearly provides supporting evidence. However, validity issues with meta analysis as we assume that all studies are held to the same scientific standards. However bonus points of global references.
The Dopamine Hypothesis
Neurotransmitters
These are the brain’s chemical messengers that appear to work differently in the brain of a patient with schizophrenia.
In particular a transmitter called dopamine.
Dopamine is important in the functioning of several brain systerms.
Hyperdopaminergic in the subcortex
The original version of the dopamine hypothesis focused on the possible role of high levels of activity of dopamine in the subcortex.
For example, an excess of dopamine receptors in Broca’s area may be associated with poverty of speech and/or the experience of auditory halluncinations.
Hypodopaminergia in the cortex
More recent version of the dopamine hypothesis have forced instead on abnormal dopamine systerms in the brain’s cortex rather thann subcortex.
Goldman-Rakic et al 2004
Have identified a role for low levels of dopamine in the prefrontal cortex which is responsible for thinking and decision making, in the negative symptoms of schizophrenia.
This is the second explanation developed
It claims that it is not excessive dopamine that causes schizophrenia but instead the reuslt of more dopamine receptors.
More dopamine receptors lead to more firing and Andover production of messages.
Owen et al 1987
Found a large numbers of dopamine receptors in autopsies of schizophrenia individuals.
Neural Correlaties of Schizophrenia
Neural correlates
These are measurements of the structure or function of the brain that correlate with an experience,, in this case schizophrenia. Both postive and negative symptoms have neural correlates.
Neural correlates of negative symptoms
One negative symptom is abolition.
It involves the loss of motivation.
Motivation i moves the anticipation of a reward.
For example, the ventral striatum is believed to be particularly involved in motivation.
it therefore follows that abnormality of areas like the ventral striatum maybe involved in the development of abolition.
Juckel et al 2006
They have mreaured acitvity levels in the ventral striatum in schizophrenicss.
Found…
Lower leaves of activity than thawed observed in controls.
They observed a negative corrections between activity levels in the ventral striatum and the severity of overall negatives symptoms.
Neural correlates of positive symptoms
Postivie symptoms also have neural correlates.
Allen et al 2007
They scanned the brains of patients experiencing auditory halluncations and compared to a control group.
They found…
That lower activations levels in the superior temporal gyrus and anterior cingulate gyrus were found in the halluncation group, who also made more errors than the control group.
We can thus say that reduced activity in these areas of the brain Ian’s neural correlates of auditory halluncaitons.
Specific brain areas involvement
Prefrontal cortex
The prefrontal cortex aka. PFC is involved in executive control for example, reasoning, judgement and planning.
It has been hypothesised that the cognitive symptoms of schizophrenia result from deficits within the PFC.
The hippocampus
Several studies have respirated anatomical changes in the hippocampus in schizophrenia patients.
Goto and Grace
Suggests that hippocampus dysfunction might also influence levels of dopamine relapse and indreiciltiy affecting the processing of information.
Grey matter
Individuals with schizophrenia have a reduced volume of gray matter in their brain.
Researchers have found that many people with schizophrenia have enlarged ventricles.
Large ventricles are thought to be a consequence of when the brain is not developing properly.
Cannon et al 2014
Found that individuals at high clinical risk who developed schizophrenia showed a stepper rate of gray matter loss and a greater rate of expansion of brain ventricles
White matter
White matter found in the brain and spinal cord is made up of nerve fibres convered in myelin,
Myelin creates an insulating stealth around nerve fibres and ensures efficient information processing.
Du et al 2013
Found reduced myelination of white matter pathways in schizophrenia patients.
Arguably
Both the dopamine hypothesis and genetic factors cause schizophrenia.
Benzel et al in 2007
Found three genes that have been asssociated with excess dopamine in specific D2 receptors, leading to postive symptoms.
The genes for example were DRD4 anf COMT
This implies that it is only solely genetic or solely dopamine but instead they interact together to increase the chances of schizophrenia developing.