Genes as an explanation for Schizophrenia Flashcards
Who is at highest risk of getting schizophrenia?
A person with a schizophrenic identical twin, 40-65%
What is the role of the 22q11 gene in schizophrenia?
Patients with a 22q11 depletion (section of it missing) show symptoms similar to those of schizophrenia, 18% risk of SZ
What other gene has potential importance in the development of schizophrenia?
DISC1
What is an alternative idea to individual genes?
Variants (alternative forms of genes) that occur within the groupings of certain genes contribute to the disorder, e.g Xq23
What supports the idea that variants that occur impact SZ?
Kirov et al 2008 - 52% of cases of sz had the Xq23 variant when it wasn’t found in 372 controls
How could adolescence contribute to schizophrenia?
At adolescence the brain prunes itself by removing unnecessary synapses, if a gene is inherited (C4) then excessive amounts of synapses may be lost leading to cognitive symptoms
How is genes as an explanation for SZ reductionist?
It only focuses on genes to explain an entire disorder rather than taking multiple factors like the environment into account.
What is a methodological advantage of this theory?
There are many different methods that are used to study the effect of genes on the disorder, including family studies, twin studies and DNA pooling. Reliability ++
Application to real life?
Future treatments designed to suppress excrssive levels of pruning by counteracting runaway C4 in at risk individuals might prevent a process that could otherwise develop into a psychotic illness.
How does Xu et al (2008) support this theory?
They examined 1077 people, 152 with SZ and their parents, 10% of the patients had a mutation that differed their DNA from their parents compared to 2% - suggests mutation
What is a limitation with the theory concerning the family?
Many people with sz don’t have a family member with the disorder and many people with family members who have SZ don’t have it
How does Gottesman and Shields (1966) support it?
MZ and DZ twins comapred for sz, concordance rates: MZ - 42%, DZ - 9% suggesting a genetic componant to sz,
What is a limitation of Gottesman and Shields (1966)?
Concordance rates for MZ were not 100% suggesting there is an environmental element.
How does Inouye (1961) support the theory?
They found a 74% concordance for people with progressive chronic sz and 39% where twins had mild transparent schizophrenia.
