biological exp for schiz

Question 1

what is the genetic basis

Answer 1

-family studies = large scale (gottesman). risk of developing schz increases in line w genetic similarity to a relation w the condition
- e.g hv aunt w shz = 2% chance
sibling has it=9%
identical twin. = 48%
families share aspects of same env too

Question 2

what do adoption studies show

Answer 2

-studies of generically related individuals reared apart
- TIERNARI ET AL= finland study 164. adoptees whose mothers had been diagnosed w SP
- 11(6.7%) also received a diagnosis of SP
- compared to js 4(2%). of the 197 control adoptees (. whose mother didn’t have schz)

Question 3

what are candidate genes role in sp

Answer 3

• implicated in the development of SP

Question 4

how do we know SP is polygenic

Answer 4

-bc it’s not js due to one single gene but a few around 108 genes

Question 5

what did ripke say about candidate genes

Answer 5

• he combined data from genome wide studies where they looked at whole human genome vs particular genes of SP
  -genetic makeup of 37,000 patients were compared to 43,000 controls who did have SP
  -108 Seaparate generic variations were associated w increase risk of SP

Question 6

what genes were associated with increased risk of SP

Answer 6

-Coding of functioning of a number of neurotransmitters including dopamine

Question 7

how does SP appear to be aetiologically heterogenous

Answer 7

-diff combinations of factors including genetic variations may lead to the condition

Question 8

what’s the role of mutation

Answer 8

-sp can have genetic origin even if absent in the family
-explained by mutuation in parental DNA caused by radiation, position or viral infection

Question 9

how is there evidence of role of mutuation

Answer 9

• positive correlations between parental age (associated with increased risk of sperm mutation
  -risk of SP increasing from 0.7% w fathers under 25 to over 2% in father over 50 y/o
  (brown et al 2002)

Question 10

what are the strengths of the genetic basis

Answer 10

(research support)
-gotesman show genetic similarity increases risk of SP
-TIERNARi shows biological kids of parents with SP are at risk even in adoptive family
- recent twin study HILLIER ET AL= showed concordance rate of 33% for identical and 7% for non identical
some people more vulnerable to SP due to genetic makeup

(expansion for research support )
-but if genes were the only cause of SP then the percentages should be 100%
-theory is too deterministic js bc we are “predisposed” by our genes we cannot necessarily get the disorder
-concordance rates in families may js be more due to the common rearing patterns or other env factors that hv nothing to do with heredity

Question 11

weaknessss of genetic basis

Answer 11

(env factors)
-env factors induce biological and psychological influences, biological risk factors include birth complications and smoking cannabis in teenagers (di forti et al)
-childhood trauma leaves ppl more vulnerable to adult MH evidence to specific link to SP
- MORKVED ET AL= found 67% of ppl w SP decided psychotic condition claimed at least one childhood trauma opposed to. 38% of matched pair group w non psychotic so genetic factors can’t provide exp alone

(adoption studies)
-only reveal small percentage
-only in finland tiernari= can’t always be generalised

Question 12

eval extra for genetic basis

Answer 12

(genetic counselling)
- application for understanding of likely role genes play in SP
-if one or more parents have a relative w SP risk of having a child w Sp increases
-risk estimate is an average figure
-but env also matters
- so it’s not a complete picture

Question 13

what are the neural explanations for schizophrenia,

Answer 13

-patterns or structure of activity in the brain that occur in conjunction w an explanation may be implicated in the origins of that experience

DOPAMINE best known neural correlate with shizo

Question 14

what’s the original dopamine hypo

Answer 14

• based on the discovery of anti psychotic drugs used to treat SP
  -which reduce dopamine caused by symptoms similar to ppl w parkinson’s disease a condition linked to low dopamine levels
• so Sp may be caused by high dopamine high levels
  (hyperdooaminergia) in subcortical areas of the brain

Question 15

example of dopamines correlation w SP

Answer 15

-excess of dopamine receptors in the pathways from subcortex to broca’s areas (resp for speech production ) may explain some symptoms of SP e.g speech poverty and avoiliton)

Question 16

what’s the updated version of the dopamine hypo

Answer 16

-DAVIS ET AL - proposed addition of cortical hypodoomanergia
low dopamine in the brain cortex to explain symptoms of SP
-e.g low levels of dopamine in pre frontal cortex (resp for thinking) could explain cognitive issues i.e negative symptoms of SP and cortical hypodopminergia leads to subcortical hyperdopamingeria

Question 17

what can we conclude about dopamine

Answer 17

-both high and low levels of dopamine in diff religions may play a role

Question 18

how can we explain simply

Answer 18

-excess dopamine subcortically is associated w positive symptoms
-deficit of dopamine in cortex associated w negative and cog symptoms of SP
-cortical hypoamingeria leads to subcortical hyperdopaminergia

Question 19

what’s the updates versions of dopamine.

Answer 19

-current versions of the dopamine hypo also try to explain the origins of abnormal dopamine function
-genetic variation and early experiences of stress both psychological and physical makes some people more sensitive to CORTICAL HYPODOPERMENRGIA AND SUBCORTICAL Hyperdopamjnergia
(howes et al 2017)

Question 20

strengths of neural correlates

Answer 20

(evidence to support dopamine)
-amphetamines increase dopamine and worsen symptoms in people w SP and reduce symptoms in people without
-anti psychotic drugs reduce dopamine and reduce symptoms intensely
-some candidates genes act in the production of dopamine
so dopamine is involved w SP

Question 21

weaknesses of neural correlates

Answer 21

(glutamate)
-post mortem and live scanning studies hv consistently found raised levels of glutamate in several brain regions of people w SP (MCCUTHEON ET AL)
- several candidate genes for SP are believed to be involved w glutamate production
- result strong case can be made for the role of other neurotransmitters

Question 22

what can we say about amphetamines psychosis

Answer 22

• TEHN ET AL= induced SP like symptoms in rats using amonetamines and then relieved symptoms using drugs that reduce dopamine action
  supports dopamine hypo
  but other drugs that also increase dopamine do not cause SP symptoms (DEPATIE AND LAL 2001)