Biological Explanations

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  • Created by: FatCat3
  • Created on: 05-02-23 17:23
what are the 2 genetic explanations of s?
1.suffers have inherited s from their parents
2.specific genes cause the illness
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how has s been seen to be genetic?
through family studies that indicated that the closer to the genetic rs to someone w s, the higher the chance of developing the disorder
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what did a researcher report about s in family studies?
Gottesman found that although s only 1% go population, chanced of first degree relatives ie parents/siblings developing chance is 12%, (+if both parents have s, 40% chance a child of theirs will have s)
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what have twin studies shown
that mz twins have an increased concordance rates then dz twins indicating that there is a degree of heritability as both twins share the same environment but mz twins still have a genetic make up
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what did other researchers find of twins studies?
Gottesman and shields find a concordance rate of 42% of mz and 9% of dz
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what did the Maudley Twin Register find and which psychologist was it?
cardno et al forbid 40% of concordance rates in mz twins, 5.3% in dz twins
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whats one issue ion comparing concordance rates?
whats a solution of thus?
cr between then same family is that they also share the environment so its difficult to isolate the effects of environmental and genetic factors
-use twins from adoptive studies as can compare between bio and adoptive parents
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what did another piece of research find?
Heston compared 47 children of s mothers who had been fostered/adopted in first month compared to a control group of 50 children who were raised in same home as children, none of the control group developed s but 17% of children w-
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continuing w previous card
-bio s mother s developed s (+were also prone to developing other abnormalities or involved in criminal activities)
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-specific gene-
what is also know a ?
polygenic as there are a no. of gene in s, diff studies have identified candidate genes which makes aetiologically heterogeneous ie s caused by many diff genes
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what did another researcher find about DNA?
Miyakawa et al studied DNA from those affected by s and found those w s were more likely to have a defective version of a gene called PPP3CC acossaiaateod w production of calcineurin regulating immune system
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what did another researcher find?
Sherrington et al found a gene located on chromosome 5 linked to a small no of extended families w the disorder
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name the evaluation
-cant be sole factor since cr for mz twins is between 40-60% but not 100% (+reductionist)
-nature vs nurture ie maybe mz twins are treated similarly growing up compared to dz twins, confiding behaviour
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continuing w previous card
-family studies uses retrospective data that relies on memories- inaccurate data,prospective data is better
-2/3 of ppl w s dont have a relative w a similar diagnosis dont inherit- may be a mutation in paternal DNA caused by radiation, etc
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what us the dopamine hypothesis?
one of the chemicals/NT in the brain causes neurons to fire
one of chemicals responsible for transmitting signals between neurons in brains
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what did the original d.h argue?
that s was caused by excessive amount activity of dopamine causing neurons to respond and dopamine to fire too often, this transmits too many messages which can cause overload and produce too many symptoms of s
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what happens as a result of this?
what did another researcher find?
s caused by high density of dopamine receptors and high sensitivity in dopamine receptors causing messages form neurons to fire too often
snyder says too much dopamine in synapse can lead to s
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what are the 2 variations of the dopamine hypothesis and example it?
.hyperdopaminergia in the subcortext- the original version of hypothesis focuses on the high levels of dopamine in s, central area of brain, ie high dopamine in brocas area associated with poverty of speech/ auditory hallucinations
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continuing w previous card
.hypodopaminergia in the cortex- more recent version focuses on abnormal dopamine systems in brain cortex- esp drefrotnal cortex responsible for thinking+decision-making explaining negative symptoms
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what psychologist updated the theory and why?
Davis et al cuz he found high levels aren't found in all s, modern anti-s drug clozapine w very little dopamine blocking is effective
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name the evaluations
-never drugs ie clozapine more effective then traditional ones which effective multiple N.T, D.H too simplistic
+practical applications to effective treatment ie clozapine more effective than neuroleptics at-
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continuing w previous card
-relieving s, improving patient's quality of life
+s sufferer have more support D.H Owen et al found from autopsies, s ppl have more d receptors
-not present in all s esp those w negative symptoms, +cause-effect issue
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what does neural correlates believe in?
believes s developed due to structural and functional brain abnormalities ie specific brain areas are associated w the disorder development
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why was the evidence limited prior?
why is evidence better now?
because researchers used post mortem examinations to conduct research on dead s
-now due to technological advancements firms can take pictures of brain in action by non-invasive scanning, this allows functioning brain of-
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continuing w previous card
-s to be compared to non-s to see which brain areas are connected to s as can see their working memory/processing task, etc
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what does this explanation propose s is caused by?
enlarged verticals, fluid-filed gap between brain areas, ev associated w damage to central brain areas+pre-frotnal cortex, such damages are associated w negative symptoms
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what did a researcher find linked to enlarged verticals?
Johnstone found s had ev while non suffers didn't, showing s may be related to loss of brain tissue
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name the evaluation
-ev may only explain certain s symptoms, weyandt reported that ev associated w negative symptoms, only applied to specific types of s
-research into ev is inconclusive as some non s have ev while not all s have ev
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continuing w previous card
-s dont respond to medication are those ev meaning it is an effect of suffering for a long period of time ie is it the s causing long term physical brain damage rather then the brain damage causing the s, ev could be cause not consequence
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continuing w previous card
-research indicating structural brain damage is often evident at first onset of s, performing longitudinal study shows its possible to assess whether damage worse as it continues. Ho et al performed MRI scans on recent onset s and-
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continuing w previous card
-rescanned them 3 years later, found evidence of brain damage which worsened over time even though they were on medicine, suggesting brain damage does increase in s area over time
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Card 2

Front

how has s been seen to be genetic?

Back

through family studies that indicated that the closer to the genetic rs to someone w s, the higher the chance of developing the disorder

Card 3

Front

what did a researcher report about s in family studies?

Back

Preview of the front of card 3

Card 4

Front

what have twin studies shown

Back

Preview of the front of card 4

Card 5

Front

what did other researchers find of twins studies?

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