Schizophrenia- explanations- biological Flashcards

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1
Q

genetics

A

we inherit 50% or our genes from each parent, genes code for proteins that create our brains and the neurological networks that make up our mental states including psychopathology. so SZ can be inherited

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2
Q

diathesis stress model

A

genes- the diathesis- put someone at risk and the stress is the environment that determine who develops the disorder and when. until the 1960s researchers believed sz to be wholly genetic but in recent years it is believed there is an interaction effect. those without the genes will not develop the disorder no matter the environment but those with the genes are affected by environmental stressors.

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3
Q

liability threshold model

A

behavioural geneticists behaviour that there are a number of genes that are involved in SZ- some possessing greater effect than others. the more of these genes the individual possesses the greater risk of SZ.

prior to this model sz was believed to be caused by a single gene, others have thought that several genes in combination were the sole cause.

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4
Q

combining the diathesis stress model and liability threshold model

A

those with a higher liability threshold will be more at risk at developing SZ as it will require fewer stressors to trigger onset, whilst those with lower liability threshold require greater or more major stressors for onset (which can be protected against with the right knowledge)

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5
Q

twin studies outline nature of them

A

if genetics are important
expect higher concordance rates in MZs than DZs because they share all the same genes whereas the later share only half.
natural experiment
IV: degree of genetic similarity
similarity of parenting is controlled within each pair of twins the parental behaviour is likely to be similar

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6
Q

adoption studies outline nature of them

A

if genetics are important
expect higher concordance rate between adopted offspring of parents with Sz and their biological parents

usually theres a control group of adopted offspring of parents without SZ for possibility that adoption itself can contribute to SZ

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7
Q

separated twin studies outline nature of them

A

if genes important
concordance between separated MZs should be high
anything above baseline rate (1%) the higher the influence of the genes

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8
Q

molecular genetics outline

A

if genes important
expect to identify specific genes that increase risk of SZ
likely to be a number of genes
may act in isolation or combination leading to different combinations of symptoms

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9
Q

twins studies results and examples
(and 1 sep twin stud)
bullet point PPE

A

twin studies show genetic component of SZ and nearly all studies show that MZ twin concordance rates are higher than DZs. e.g.
gottesman review
meta analysis essentially (pooled results from 40 twin studies)
40 paris of twins
pooled concordance rate for MZs was 48% and the DZs 17%

gottesman also did a seperated twin study for 14 pairs of twins MZ concordance was 58%
Very small study but is consistent with findings of other twin studies

Kendler
MZs 53%
DZ 15%

overall and from recent findings

mz twins generally 41-65%
Dz twins generally 0-28%

since this evidence comes from a number of meta-analyses is it particularly strong- the results are less likely to be flukes because they’ve been pooled from large number of studies and MZ and DZ twins and conducted at different times in different studies thus providing strong and consistent support for the genetic explanation.

consistent evidence from a series of reviews for a strong genetic effect

however as genes are clearly not the only factor (never 100% concordance) provides room for environmental effect- for example int he diathesis stress model

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10
Q

Adoption studies results and examples

bullet point PPE

A

tienari et al

Finnish adopted children who had SZ mothers had a 7% chance of developing sz compared to 1.5% of the controls (who were adopted children without SZ mothers)

the risk for developing sz was 4 times greater for adopted children with SZ bio mothers than it was for adopted children without SZ bio mums

adoptees at moderate-high genetic risk are siginificantly more sensitive to adverse rearing patterns in adoptive families than are adoptees at low genetic risk

fewer adoption studies but they do consistently suggest a moderately strong genetic effect. there is still a high risk of developing sz despite being raised by someone other than the biological mother suggesting it’s genetic

Wahlberg re examined tienari’s findings and found a strong environmental effect for those at risk of developing SZ who were adopted into families with poor communication.

providing direct support for the diathesis stress model of Sz

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11
Q

molecular genetics

A

research has shown links between a large number of genes which appear to have small effects many of them related to dopamine dysfunction. D2 receptor gene in particular (glut et al)

Allen et al 2008
across a meta analysis 24 genetic variants in 16 different genes (including DRD2) showed to increase risk by 23%

4 of the top 10 gene variants most associated with sz are directly involved in dopaminergic pathways.

a particularly influential gene variant is one that affecting monoamine transporter protein who’s role is to package dopamine and other monoamines into vesicles (an increasing risk of 63%) when this protein is over active it means more dopamine is being released into the synapse and therefore binding to DRD2 receptors on the post synaptic membrane.

providing support for the liability threshold model, as not just one gene is increased and increases in risk are small

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12
Q

methodological issues in research with twin studies

A

more similar environments for MZs than DZs

may be treated more similarly because they look more alike
it could be that preteens feel more obliged to treat mss similarly because of the perception that they are very similar, whereas this is not he case with DZs
this could therefore mean that there is an environmental reason for the higher concordance rates rather than the genetic reason, which flaws the twin study method (and separated twin method solves)

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13
Q

methodological issues with adoption studies

A

selective placement

it is possible that children with history of SZ may not be chosen by better informed and potential more contentious parents meaning that those children are instead placed in more psychologically harmful adoptive homes.

this could account for higher concordance rates of s than in control cases, children with S parents may be placed in homes which are more stressful therefore more likely to develop sz

the similarly of the offspring and the sz mother is therefore better explained the the environmental factors, is this criticism is justifiable. A lot of assumptions have been made in relation to pickiness and quality of parenting. a relationship which may exist in some cases but not all and not to the extent of discrediting the genetic effects

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14
Q

to what extent have the findings on the effect of genetics been triangulated?

A
a number of different studies:
twin
adopted
sep twin
genetics

all shown the same result- genetics play a role

CR higher for MZs in all cases
and specific genes have been identified as creating risk

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15
Q

to what extent have the findings of the effect of genetics been replicated /assessed in MA??

A

(the best)
twin studies- lots of replication - gottesman review of 40 twin studies
adoption studies - 6 studies
separated twin studies (only 14 pairs which gottesman collected) (the worst)
molecular genetics provides vast evidence as this is more objective.

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16
Q

the dopamine hypothesis

A

suggests a role for dopamine for the aetiology (causal pathway) of schizophrenia

the precise nature of D in creating sz is debated.

the hypothesis developed out the success of treatments for S that worked by affecting dopamine receptors.

the problem is:
an excess of dopamine neurotransmitter
an excess of the dopamine receptors (e.g. DRD2)
over sensitivity of the dopamine receptors

17
Q

problems of causality of D

A

does DD cause SZ
does SZ cause DD
or something else cause DD/SZ

evidence is only correlational, so casual claims cannot be made

18
Q

what are the two pieces of evidence that do in fact suggest a cause and effect of dopamine and sz

A

1) L dopa- a drug which increases dopamine levels leads to SZ like symptoms in previously affected parkinson’s patients
2) recreational use of amphetamines, which also increase dopamine levels induce S like symptoms. (and they worsen symptoms in those with S)

19
Q

inconsistency of findings for the dopamine hypothesis

A

major problem is that the hypothesis doesn’t apply to al SZs
drug treatments don’t help everyone
not all users of amphetamines or L dopa develop S like symptoms
dopamine does not seem to be involved in type 2/negative symptoms of SZ

20
Q

howes and kapur

A

argue that dopamine is the final common pathway that produces psychotic symptoms (positive/type 1)

all SZ or ppl with other disoders who have psychotic symptoms have presynaptic dopamine dysfunction

so actually the theory is an explanation for psychosis rather than sz (as it is currently categorised and diagnosed)

21
Q

DD: initial causes of the dopamine dysregulation according to howes and kapur (2008) a reviewed version of the dopamine dysregulation- final common pathway

1st point made!

A

multiple factors including those of genetic and environmental origin, interact and result in the DD

  • genes
  • stressful life events
  • family factors e.g. expressed emotion
  • drug taking
  • unemployment
  • lack of close friends
  • abuse in childhood

these hit have different strengthes and combine in diverse ways

the reason for unique symptoms is because of the unique pathways from the initial causes to the presynaptic DD

addressing a problem of causality- that the DD comes from multiple factors.

supports the idea that different patients with psychosis have a unique path of causation there experience a unique condition

22
Q

DD: locus of dysfunction

Howes and kapur (2008) review of dopamine hypothesis- final common pathway

2nd point made

A

since the locus of DD is thought to be presynaptic meaning there is over active protein synthesis creating excess neurotransmitter and increased tendency to release it into the synapse (the dysfunction is not at the receptors according to the final common pathway version of the dopamine hypothesis)

implications of this point is that current drugs target downstream (so at the post synaptic membranes of neurones) at the receptors.
they are therefore not treating the primary location of the abnormality which is why they are only partially effective for some people and for others make symptoms worse.

this suggests that drug developments need to focus on the very site of the dysfunction either through upstream effects or directly to treatment psychotic symptoms.

23
Q

DD effect on psychotic symptoms

howes and kapur (2008) review of dopamine hypothesis- final common pathway

3rd point made

A

DD is specifically linked to the dimension of positive psychotic symptoms and psychosis proneness rather than sz.
however the exact diagnosis reflects the nature of the hits coupled with sociocultural factors and not the dopamine dysfunction per se.

since the theory only explains psychosis, current diagnostic systems for psychotic disorders should be revised to emphasize symptom dimensions being seen as independent (having it’s own underlying mechanisms) as BENTALL argues?

24
Q

DD psychological effects

howes and kapur (2008) review of dopamine hypothesis- final common pathway

4th point made

A

DD alters the appraisal of stimuli through the process of aberrant salience (stimuli that are not relevant are taken as relevant).
SZs have difficulty telling the difference between what’s relevant and what’s irrelevant

they make sense of experiences in the usual way but because they can’t filter out irrelevant info their thoughts get confused

leading to psychosis

a clinical implication is that the person who formed the delusional belief is as sure about that belief as they are about a non-psychotic belief (why shouldn’t they be, they were formed in the same way, it’s just one incorporated information that wasn’t salient).

25
Q

Nature/nurture debate for sz dopamine hypothesis

A

Howes and kapur see the dd to be the common mechanism in all SZs

and the precise cause of the dysregulation is a mixture of genetic and environmental factors (including EE and stressful life events)- each making it’s own contribtuion to the dysfunction.

this is the opposite to what behaviourist geneticists believe (the diathesis-stress model) which is that all sz has some genetic basis

with the dopamine hypothesis- sz can develop without any genetic influence s long as the hits on dopamine functioning were strong enough.

26
Q

Howes and kapur reviewing the dopamine hypothesis what’s good about it/what does it solve.

A

new version deals with the problems of drugs not being effective (but not for all patients because the mode of action isn’t always in the same place)

explains why negative symptoms are unrelated to dopamine and that treatment targeting dopermingeric pathways is unsuccessful.

DD leads only to psychosis (positive symptoms- delusions and hallucinations)

27
Q

A02 dopamine hypothesis howes and kapur 2008

claim: multiple factors

Give evidence

A

dopamine is the common pathway through which psychosis develops whether it be through genetic or environmental causes

1) the genes that most strongly associate with schizophrenia are those within the dopaminergic pathways (4 of the top 10 gene variants according to a databse on the SZ Research Forum)
the gene variant with the stongest association is one that affects the vesicular monoamine transporter protein

2) environmental factors associated with increase: unemployment, lack of close friends and social networks and childhood abuse are linked to social isolation and subordination, in animal studies these have lead to dopamine dysfunction.

these affects are of use since similar ones have been found in humans- people who reported low maternal care as a child dopamine in response to stress was increased suggesting the environment can affect the dopamine system

genes and environment interact not just in isolation

28
Q

ao2 dopamine hypothesis howes and kapur 2008

claim: locus of DD

give evidence

A

In a meta analysis of brain scanning studies HK found higher rates of presynaptic DD in szs while other DD (i.e. at post synaptic membranes and at the synapse itself seemed less pronounced.
large effect size of 0.79

concluded that the largest Dopaminergic abnormality in sz is presynaptic affecting the dopamine synthesis capacity, the dopamine level and the dopamine release.

current drug treatments act at the D2 receptors which fail to treat the abnormality

supportive of new dopamine hypothesis version

29
Q

Ao2 DD linked to dimension of positive/pschotic symptoms, psychotic proneness

h&k 2008

A

the evidence shows that szs with psychotic show DD while those without do not!
and non szs with psychotic symptoms also have DD

so DD is related only to positive psychotic symptoms which is not the full picture for SZ but has explanatory power for those with positive symtoms of the disorder.

drugs that reduce positive symptoms all work on the dopamine system.

in over 120 neuroimaging studies have investigated the in vivo effects of antipsychotics treatments on dopamine receptors in sz. these show that at clinical doses all licensed AP drugs block the D2 receptor

30
Q

DD alters the appraisal of stimulus thought the process of aberrant salience
ao2 HK

A

experiments by Berridge and Robinson among others have implicated a distinct role for dopamine systems in motivated salience and reward prediction- linking the neurochemical dysfunction to the clinical expression of salience.