Bio explanations of schizophrenia- Genetic

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  • Created by: imanilara
  • Created on: 29-02-16 18:56

Intro+Family studies AO1

-Sz is an inherited disorder- inheritance of faulty genes
-genes have caused brain to develop in diff way than someone without Sz
-different neuroanatomy or neurophysiology

Family studies:
-Eg Gottesman 1991 look at whether the biological relatives of someone w Sz are more likely to get the disease than controls- this has support for genetic compnent in Sz

-Seen in studies- risk of Sz is directly proportional to the amount of genes they share w the sufferer

-Child w two Sz parents -46% concordance rate, mz twins 48%

-Chid w one parent- 13% concordance rate

-Sibling- 9% concordance rate 

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Family Studies AO2

-Suggests there is a genetic element in Sz, although it should be noted that all families share the same environment too
-No 100% concordance in mz twins- must be some other factors too
-To make progress in distinguishing between environmental and genetic factors, we can use twin/adoption studies

Gottesman- 63% of Sz sufferers do not have any family members w disease- shows that in many cases it doesn't seem to be genetic 

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Twin studies AO1+AO2

Twins usually share the same environment, so any difference in concordance rates can be put down to genetics

Joseph (2004)

-metanalysis for all Sz twin studies before 2001 showed concordance rate of 40.4% for mz+ 7.4% for dz
-more recently, methodologically sound studies (using blind studies), where the researchers do not know whether the twins are dz or mz produce lower concordance rates. Study suggested higher control decreases the concordance. However mz still higher than dz, showing some sz has some genetic influence

Cardno et al (2002)

MZ concordance - 26.5, dz 0%- some genetic factors, but not the only one

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Twin studies AO2

-V small sample sizes- MZ twins are rare and only 1% would be expected to have Sz
-Not all twin studies use same diagnostic criteria to diagnose Sz-different concordance rates-Mcguffin
-Not all use same criteria to distinguish between mz and dz twins (before zygotic tests could be carried out)
-Not all use same method in producing concordance rate

And so they cannot be compared

Other commentary:
Twin studies assume that mz and dz twins share the same environment and so any changes in concordance are down to genetics-however- Joseph 2004- found that mz twins may be treated differently than dz twins- they have a heightened sense of loss of identity "the twins"
-might lead to Sz symptoms- could have environmental instead of genetic factors

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Adoption Studies AO1

Family+Twin share the same environment, adoption allows the study of genetically related ppl who are reared in different environments
Seen in the Finnish Adoption study:

Tienari et al 1991- 155 adopted children w mothers who had sz-10% got it, compared to control who had no family history of Sz-1% got it

Tienari et al 2000- 164 adopted children w mothers who had Sz-6.7% got it, compared to control who got 2%

Investigators concluded that this was decisive confirmation of a genetic liability to Sz

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Adoption studies AO2

Methodological issues- different criteria for Sz used as it changes

Assumes that there is no difference in the parents that take children with such histories and others- they are a biased sample
Joseph suggested this was unlikely- they would know prior about the history of the child 

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If genetic then the evolutionary explanation should explain-genes that contribute to reproductive fitness are passed on and can be seen today
Sz in small doses could be advantageous-not in large doses as the behaviours are too extreme and do not allow a person to function adaptively 

Evidence of it in the EEA is that it is found in remote racial enclaves-Australian Aborigines-they are the most similar to those in the EEA

Stevens and Price:
-Schizoid personalities had a function
-When the group gets too big, and the only way to increase reproductive fitness is to split off, Sz characteristics of grandeur, delusion, bizarre beliefs means they have the confidence to break away and inspire others as a charismatic leader to do the same
This charisma and confidence may also be desirable and leads to greater rep. success.

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Biochemical factors - Dopamine hypothesis

-neurones fire dopamine too easily/often leading to an increase in dopamine in the brain and the characteristic symptoms of sz
-evidence from PET scans and post-mortem examinations show that people w Sz have abnormally high dopamine receptors on the neurone membrane, meaning more dopamine binding and neurone firing
-Dopamine neurones play a key role in guiding attention-disturbances in the neurones can lead to problems w attention and perception- characteristics of Sz

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Dopamine hypothesis AO2

-Amphetamines: dopamine agonists- increase the action of dopamine at the synapse
-Stimulate DA neurones, causing synapses to be flooded with this neurotransmitter
In people who do not suffer from Sz, high doses cause characteristic hallucinations+delusions associated w Sz
-In people who are suffering w Sz, high doses of Amphetamines make symptoms worse

Good evidence that high DA levels are responsible because:
Amphetemines (DA agonists) cause Sz symptoms which suggests High DA causes Sz

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Antipsychotic drugs

Antipsychotics- neuroleptics-one thing in common dopamine antagonists (Block DA activity in the brain)- reducing activity in the DA eliminates symptoms like delusions/hallucinations

This strengthens the case for the hypothesis that Sz is caused by too much dopamine because: 
Neuroleptics reduce Sz symptoms suggests high DA causes Sz

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Parkinson's Disease

-People who have parkinson's have low dopamine activity
-Degenerative disease-destroys dopamine neurones
-Gives rise to motor problems-shaking-and then cognitive+behaviour problems 
Some Parkinson's patients prescribed L-Dopa (raises DA levels) experienced Sz symptoms (Grilly 2002)

Good evidence that high levs of DA cause Sz because:
-when you raise DA levels by L.Dopa, Sz symptoms can exist 

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Commentary: WEAKNESSES

-L-Dopa and amphetamines do not worsen symptoms in all people diagnosed w Sz
-Phenothiazines-(type of neuroleptic) do not work for everyone diagnosed w Sz-only tend to alleviate positive symptoms-may be a result with of errors in diagnosis
-Post mortem examinations-carried out on individuals who have been taking anti psychotic for years-not clear whether the differences in their brains result from the disease or treatment. Haracz reviewed post mortems + found that those who showed elevated DA levels had recieved anti psychotic drugs shortly before death - evidence that it is drugs not disease 
-PET scans 
are yet to show convincing evidence of unusual DA activity in the brains of Sz sufferers-not all show increased DA receptors

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Conclusion to Biochemical Exp

It is worth noting that a proximate biological cause (raised DA levs) could be linked with an ultimate biological cause (faulty genes) or an environmental one.
It is possible that environmental causes are the ultimate explanation (ie traumatic experiences) lead to faulty brain development/functioning- raised DA levels 


-no evidence for 100% concordance in twins
-majority of sufferers (63%) have no family history
-contradictory evidence from scans and drug trials looking at DA hypothesis 

Evidence does convince on the question of whether bio factors do have influence-current researchers favour the diathesis stress model-biological predisposition but the disorder only develops if other stressors are present in the person's life  -NATURE/NURTURE

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