Biologica Explamasioms Of SZ Flashcards
What are the two main biological explanations of schiz
The genetic basis and the dopamine hyptihesis
How are genetic factors tested
Through family, twin and adoption studies
What is family studies find?
Family studies find Individuals who have SZ and determine whether their biological relatives are similarly affected than non biological relatives. Family studies have shown that the closer the genetic relatedness, the greater the risk. Gottesman found if both parents were SZ, then likelihood of offspring was 46%. If one parent then 13% then if one sibling has then it is 9% demonstrating that the closer you are the more likely you are to be SZ
What twin study used img
They are an opportunity for researchers to investigate the nature/nurture debate in terms of the contribution of hereditary and environmental influences in having SZ. MZ twins share 100% of their DNA, whereas DZ twins only share 50%. If SZ is genetic then those MZ dons should have higher concordance rate of SZ. Some guy found 47% concordance in MZ but only 17% in DZ (Gottesman)
Adoption studies
Used to argue the nature/nurture debate. E.g. when MZ are reared apart or offspring of SZ are adopted. Tienari carried out study in Finland with 164 adoptees who’s biological mothers had all been diagnosed with SZ. 11 were diagnosed with SZ compared to 4 out of 197 who were diagnosed as SZ in a control group (mothers not SZ). Suggesting a small link between genes and inheritance of SZ
What are candidate genes
There are specific genes associated with SZ but there is combinations of these genes that can result in a person having SZ. Ripke et al compared the genetic makeup of 37000 SZ patients worldwide with 113000 controls. They found 108 different combos of genes that were associated with an increased risk of SZ. crazy if you think about it 😱😱😱. These genes all had links with the neurotransmitter dopamine.
Strengths genetic basis of SZ
Lots of research to support this basis. Gottesman, Joseph’s and Tienaris study. Thus there is a link between SZ and genes. More likely to develop SZ if come from parents of SZ than those who don’t have SZ. Highly controlled variables - cause and effect controlled for we know that genes are responsible for development of SZ
Weakness SZ genetic basis
Problems with twin and family studies is separating the nature from the nurture. E.g. MZ twins are normally reared together and sent to the same school, wear the same clothes which makes it difficult to separate upbringing from genes. Even if we look at adoption studies that attempts to separate them, they are normally raised by a relative who my rear the child similarly to parents so these studies may not be a good comparison of nature/nurture
Diathesis stress model: there is a genetic vulnerability in SZ. But this vulnerability is likely to be triggered If there is a stress trigger in the individuals life. In other words you may be born with a gene that correspond with SZ, but if yo life kinda stress free you may not have it. Thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ
More importantly, SZ can take place in theabsence of a family history. One explanation is that there may be a mutation in parental DNA, for example in paternal sperm cells. This can be caused by radiation, poison or infection. Evidence for role of mutation comes from Brown et al’s. 2002 study which showed a positive correlation between paternal age and increased risk of SZ increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. This suggests that although no direct genes are involved, a person can still get SZ if their father was older at the time of fertilisation. This suggests that the role of nature and nurture may both play a part rather than just genes.
What are neural correlates
Neural correlates are measurements of the structure or function of the brain that have a relationship with SZ especially different regions of the brain. Neural correlates also refers to how different neurotransmitters such as dopamine and serotonin (either excessive levels or low levels) in different parts of the brain can also play a part in SZ.
Strengths neural correlates
There is research evidence to support the structural changes in the brain between SZ and non SZ such as Torrey’s study with reference to enlarged brain ventricles and Conrad’s study with regards to the hippocampus.
Furthermore, this research evidence can be validated through brain scanning which is an objective method suggesting that there is face validity to the neural correlates explanation because one can actually observe the structural brain changes that occur with schizophrenic patients – this can then help to tailor make treatments that will reduce the symptoms of SZ.
Weakness neural correlates
The problem with looking at different brain regions is the fact that there are individual differences in sufferers of schizophrenia and not all patients have deficits in the functioning of different brain regions.
Also as there are different brain regions involved in SZ, it may be difficult to pinpoint which brain region is causing the symptoms.
Furthermore, it may be difficult to establish cause and effect in terms of neuroanatomy as evidence is correlational in other words, did the sufferer have abnormalities in a particular brain region and then contract schizophrenia or did the individual contract schizophrenia and then show brain abnormalities?
What is the mist well known neural correlates
One of the best known and researched example of neural correlates is the neurotransmitter dopamine – known as the Dopamine Hypothesis
Neurotransmitters are the brains chemical messengers. These appear to work differently in the brains of schizophrenics. In particular, dopamine (DA) seems to have an important role since DA is necessary in the functioning of several brain systems. DA has also been implicated in SZ.
What is the dopamine hypothesis
Thus the dopamine hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of SZ. Thus messages from neurons that transmit dopamine fire too easily and often, leading to hallucinations and delusions.
Schizophrenics are thought to have particularly high levels of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing
What’s is hyperdopaminergia
Hyperdopaminergia in the subcortex – this is based on the original version of the dopamine hypothesis in explaining SZ – this states that there are high levels of activity of dopamine in an area of the brain known as the subcortex (i.e. the central areas of the brain). For example an excess of dopamine receptors in the Broca’s area (which is responsible for speech production) may be associated with problems in speech and/or the experience of auditory hallucinations
What is hypodopaminergia
Hypodopaminergia in the cortex – recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex. Goldman-Rakic et al, (2004) have focused on the role of low levels of dopamine in the prefontal cortex (responsible for decision making and thinking) on negative symptoms of SZ.
