schizophrenia- biological explanations

Question 1

genetic basis of sz: family studies

Answer 1

-strong relationship between the degree of genetic similarity and shared risk of sz
-Gottesman’s (1991) large. scale study
-family share environment but still indicates support for genetic view.

Question 2

who investigated family studies in sz and what did they find?

Answer 2

Gottesman (1991) large scale study
-s/o with aunt with sz has 2% chance of developing it, 9% for sibling and 48% for identical twin

Question 3

genetic basis of sz: candidate genes

Answer 3

-sz is polygenic
-also aetiologically heterogenous (risk affected by diff combos)
-Ripke wt al (2014)

Question 4

who investigated candidate genes in sz and what did they find?

Answer 4

Ripke et al. (2014) combined all previous data from genome-wide studies
-found 108 separate genes associated w slightly increased risk of sz

Question 5

genetic basis of sz: mutation

Answer 5

-sz can also have a genetic origin in absence of a family history bc of mutation in parental DNA
-correlation between parental age (associated w/ increased risk of sperm mutation) and risk of sz (Brown et al. 2002)

Question 6

who investigated mutation in the genetic basis and what did they find?

Answer 6

Brown et al. 2002
correlation between parental age (associated w/ increased risk of sperm mutation) and risk of sz

Question 7

role of dopamine in neural correlates of sz

Answer 7

dopamine (DA) featured in the functioning of brain systems related to the symptoms of schizophrenia

Question 8

original dopamine hypothesis in neural correlates of sz

Answer 8

-high dopamine activity in subcortex, associated w hallucinations and poverty off speech (excess of DA receptors in pathway linking from sub cortex to Broca’s area)

Question 9

updated dopamine hypothesis in neural correlates of sz

Answer 9

-updated hypothesis added low levels of DA in the prefrontal cortex, could explain negative symptoms

Question 10

who researched the updated dopamine hypothesis and what did they find?

Answer 10

Howes et al.
-genetic variations and early experiences of stress make some more sensitive to cortical hyperdopaminergia
-explains origins of abnormal DA

Question 11

ao3 of bio explanations of sz: strong evidence base

Answer 11

-family studies show risk with w genetic similarity. twin studies found 33% concordance for MZ and 7% for DZ (Hilker et al. 2018)
-Adoption studies (e.g. Tienari et al. 2004) show biological children of parents w/ sz are at greater risk even if they grow up in an adoptive family
-shows that some people are more vulnerable to sz bc of their genes.

Question 12

ao3 of bio explanations of sz: environmental risk factors

Answer 12

-bio risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al. 2015)
-psych risk factors include childhood trauma e.g. 67% w/ sz (38% matched controls) reported at least one childhood trauma (Mørkved et al. 2017)
-genes alone cannot provide a complete explanation

Question 13

ao3 of bio explanations of sz: support of dopamine in symptoms of sz

Answer 13

-amphetamines (increase DA) mimic symptoms (Curran et al, 2004). Antipsychotic drugs (reduce DA) reduce intensity of symptoms (Tauscher et al. 2014)
-candidate genes act on production of DA or DA receptors
-strongly suggests dopamine involved in the symptoms of sz

Question 14

ao3 of bio explanations of sz: central role of glutamate

Answer 14

-post-mortem and scanning studies found raised glutamate in people w/ sz (McCutcheon et al. 2020)
-also several candidate genes for sz believed to be involved in glutamate production or processing
-strong case can be made for role of other neurotransmitters in sz