evaluation for biological explanations for schizophrenia Flashcards
multiple sources of evidence for genetic susceptibility
there is very strong evidence for genetic vulnerability to schizophrenia from a variety of sources
The Grottesman (1991) study clearly shows how genetic similarity and shared risk of schizophrenia are closely related
Adoption studies such as that by Pekka Tienari et al (2004) shows that children of people with schizophrenia are still at heightened risk of schizophrenia even if adopted into families without a history
mixed evidence for dopamine hypothesis
support for abnormal functioning in schizophrenia
dopamine agonists, like amphelamines that increase the levels of dopamine, make schizophrenia worse and can produce schizophrenia - like symptoms in people not diagnosed with schizophrenia (Curren et al 2004)
how do antipsychotic drugs work
antipsychotic drugs on the other hand, work by reducing dopamine activity (Tauscher et al 2014)
both kinds of studies suggest an important role for dopamine in schizophrenia
Radioactive labelling studies e.g. Lindstrtum et al (1909) have found that chemicals needed to provide dopamine are taken up faster in the brains of people with schizophrenia
This evidence is to suggets the dopamine does not provide a capable explanation for schizophrenia
the correlation causation problem
although there are useful studies in flagging up particular brain systems that may not be working normally, this kind of evidence leaves some important questions unanswered
e.g. Does the visual activity in the region of the brain cause the symptoms? Logically there are other possible explanations for the correlation
A negative correlation may suggest that low activity in the ventral striatum causes avolition. But it could be that avolition means that less info passes through the stratium resulting in the low activity
Therefore, although neural correlates exist, they tell us relatively little about the cause of schizophrenia
the role of mutation
schizophrenia can take place in the absence of a family history of the disorder.
One explanation for this mutation is parental sperm cells
This can be caused by radiation, poison, or viral infection
Evidence for the role mutation comes from a study showing a positive correlation between paternal age (associated with increased sperm mutation) and risk of schizophrenia, increasing from 0.7% with fathers under 25 to over 2% (Brown et al 2002)
This implies that the idea the schizophrenia runs in the family is relatively weak
(use this as a counterpoint)