Schizophrenia- Biological explanations Flashcards
What are the 2 biological explanations for SZ
1- Dopamine hypothesis
2- Genetics
What is my FIRST choice for biological explanation of SZ
Dopamine
What are the 2 dopamine hypothesis?
1- The initial dopamine hypothesis
2- The revised dopamine hypothesis
What is hyperdopaminergia?
More dopamine production
- positive symptoms
The initial dopamine hypothesis
Hyperdopaminergia
- brain of SZ patients produce more dopamine
- responsible for positive symptoms
- excess of dopamine receptors in Broca’s area
- speech poverty, alogia/auditory hallucinations
What evidence is there to support the initial dopamine hypothesis?
Parkinson’s (neurological condition causing tremors)
- given the drug L-dopa
- raised dopamine activity in the brain, reducing their symptoms
- patients began to develop SZ symptoms
How can we criticise the initial dopamine hypothesis?
Too simplistic
X only effective for reducing positive symptoms not negative
X further complicated by discovery of several subtypes of dopamine receptor sites(D1-D5)
X spread in both cortical (cerebral cortex) and subcortical (limbic system) areas of the brain
What is the revised dopamine hypothesis?
Most recent versions of the dopamine hypothesis have focused instead on the limbic system
Hyperdopaminergia AND hypodopaminergia
What are the 2 main nerve pathways?
1- Mesolimbic pathway
2- Mesocortical pathway
Leave the limbic system to other subcortical structures and the cerebral cortex
1- Mesolimbic pathway (positive symptoms)
Hyperdopaminergia
- carries signals from WTA to NACs
- too much dopamine (fire too often or quickly)
- cause overstimulation and positive symptoms
e.g. hallucinations/delusions
- antipsychotic drugs reduce dopaminergic transmission and dopamine activity in this pathway
2- Mesocortical pathway (negative symptoms)
Hypodopaminergia
- carries signals from VTA to frontal lobe
- nerve pathway vital in emotional responses, motivation and cognitive impairments
How does Davis support the mesocortical pathway?
Too little dopamine (hypofunction) is evident in d1 receptors of the frontal lobe of many individuals with the cognitive impairments and negative symptoms of SZ
Evaluation: Dopamine hypothesis
- Supporting evidence
Those who suffer from Parkinson’s disease given the L-dopa drug
- raised their dopamine activity in the brain, reducing their symptoms
- began to develop SZ symptoms
- suggests increased levels of dopamine contribute to SZ symptoms
X too simplistic, fails to account for negative symptoms
X further research into this is needed
Evaluation: Dopamine hypothesis
- Practical applications
Influenced the development of drug therapy, 1st generation antipsychotics as dopamine antagonist target the production of dopamine
- effective against positive symptoms
- phenothiazines 75% given drug were much improved compared to 25% placebo(48% worse)
- successful treatment, useful explanation
Evaluation: Dopamine hypothesis
X Reductionist
Biologically reductionist
X too simplistic to suggest SZ is only caused by dopamine, reduce solely down to NT level ignoring environmental factors
- allows for scientific study, pin point one part to develop successful treatment
- benefits allows us to understand a potential cause of SZ from a scientific viewpoint
What is my SECOND choice for the biological explanation of SZ
Genetics
Intro to genetics
Closer the biological relationship, higher the risk
- 1st degree, share 50% of genes (siblings, parents)
- comparison of SZ rates- family members
Family studies- Gottesman
MZ- 48% DZ-17% Parents-6% Sibling-9%
- indicates haring of a gene
- differences between must be caused by environment, concordance rates aren’t same
Twin studies
Gottesman and Shields MZ-42%, DZ-9%
Cardno et al- MZ-40%, DZ- 5.3%
Likely identical twins share a gene that causes SZ
DZ- same environment, genes play a part, significance of genes role
X not 100%, some other factors
Adoption studies
Heston- 10% SZ mothers, control group none
Tienari et al- 7%, 1.5%
- separates nature vs nurture
- those with SZ biological mothers more likely
- underlying biological basis
- shows reliability, similar results and findings
Candidate genes
a faulty gene that could explain SZ, polygenic
- number of genes identified which are linked
- aetiologically heterogeneous- cause more than one combination
- code for transmission for different NTs including dopamine
Complement component 3 (C4)
Researchers from MIT and Harvard identified gene that increases risk of SZ
- involved in elimination connections between neurons- process called ‘synaptic pruning’ happens naturally in humans in the teen years
What is synaptic pruning?
Getting rid of neural connectivity
How does synaptic prunin explain he onset of SZ?
It is possible that excessive or inappropriate ‘pruning’ of neural connections could lead to the development of SZ, which would explain why SZ symptoms often first appear during adolescence
Evaluation: Genetics
- Research Support
Numerous twin studies have shown a genetic link
Gottesman- CR higher for MZ twins (48%) DZ(17%)
- supports as MZ share more genes
X purely genetic expect 100%
X twins raised similarly, not separate nature v nurture
X ignores environmental, affects validity
X research is flawed, remain critical cannot solely rely upon it
Evaluation: Genetics
- Newer research
Newer technology can be used to identify certain genetic mutations
- gene mapping technology, specific genes that could increase risk of developing SZ, SEDTD1A- only found in SZ patients
- gene therapy (modification
- gene counselling (screening) possesses the gene
- preventative measures and treatment
X ethical- promoting eugenic ideas
Evaluation: Genetics
X Can’t be attributed to a single gene
SZ is polygenic (number of different genes)
X O’Donovan- identified 108 specific locations in the human genome that are linked with SZ
X even though the potential genes involved in SZ may have been identified, how they actually cause the illness is unknown as yet
X although there may be a genetic basis, it is a complex matter and more than just a few abnormal genes
