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9 Cards in this Set
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AO1 What is the Genetic explanation of schizophrenia? |
It suggests that schizophrenia is heritable so the person is born with a biological predisposition to develop it due to abnormalities. Involves a combination of genes rather than a single gene. Individuals develop schizophrenia at a rate higher than the incidents rate in the general population when a relative also has it; the closer the relative is the stronger the chance of getting schizophrenia. |
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AO2 Genetic Explanation Supporting Evidence |
Gottesman et al- Meta analysis of 40 twin and family studies. Founs a concordance rate for schizophrenia of 48% for MZ twins, 17% for DZ twins, 6% for siblings and 2% for Uncles and Aunts. Results show that there is a decline in % as the number of shared genes decline. therefore showing there is strong support for the idea that schizophrenia is a heritable illness. |
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Criticisms for Gottesman and Shields |
+ Its a reliable study a it is a meta-analysis so the same results have been found in several cases. - the concordance rate is not 100% in MZ twins, which they would be if genes were the sole reason for schizophrenia. Therefore the genetic theory is less credible as it cannot account for these discrepancies. - Environmental varibale may account of the data observed a speople who share gene also tend to share environments and may be the cause of the findings, overall weakening the internal valididty of the study. |
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Supporting evidence for genetic theory |
Tienari et al studied adopted children of schizophrenic mothers compared to a controlled group of children of non-schizophrenic mothers. They found that 10% of adopted children developed schizophrenia when their biological mother had it despite being reared separately. This shows that children who had a biological mother with schizophrenia are more likely to contract the disease, therefore supporting the idea that the more gene you share with someone who has schizophrenia the more likely you are to get it. |
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AO1 Biochemical explanation |
The dopamine hypotheses suggests an excess in activity of the neurotransmitter dopamine in the brain of those suffering from schizophrenia. There is an abnormally high number of D2 receptors on the receiving neurone so it is more activated by dopamine. This is believed to cause the symptoms experienced by schizophrenics. Dopamine is involved in controlling movements, memory, attention, problem solving and is involved in giving us feelings of enjoyment and reinforcement. |
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AO2 Biochemical explanation Supporting evidence |
Patients with Parkinsons disease who were given L-dopa (a drug which increase levels of dopamine) then suffered schizophrenic symptoms, suggesting high levels of dopamine has a role in causing schizophrenia. Similarly, amphetamines also stimulate particular nerve cells, increasing levels of dopamine. In large doses people would experience hallucinations and delusions similar to that of a schizophrenic episode. Evidence from drugs that decrease levels of dopamine further support the hypothesis. Anti psychotic medication such as phenothiazines which reduce symptoms of schizophrenia in a majority of patients within 2-3 weeks. |
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Criticisms of Biochemical explanation |
+The effectiveness of the these drugs that decrease levels of dopamine demonstrate the usefulness of the dopamine hypothesis in developing effective treatments which enable patients to live normal lives. However just because drugs that reduce dopamine relieve symptoms of schizophrenia it doesn't mean the illness was cause by abnormal brain chemistry in the first place. -Raised dopamine activity may be a symptom of schizophrenia rather than its root cause. therefore the dopamine hypothesis fails to explain why dopamine is over-active in the first place. -Anti psychotic drugs only appear to reduce the positive symptoms of schizophrenia reduce the positive symptoms of schizophrenia - therefore the negative symptoms must have some other cause, rather than being due to excess dopamine, meaning that dopamine hypothesis only partially accounts for certain symptoms of the disorder. - An alternative, more complex theory, is that dopamine increases in some neural circuits, causing the positive symptoms, while decreasing in others, causing the negative symptoms - therefore the original dopamine hypothesis is over simplistic. -Anti psychotic drugs reduce dopamine immediately, yet symptoms of schizophrenia remain for 2-3 weeks, suggesting that dopamine over-activity cannot be the only factor. |
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AO1 Other biological influences |
Neuroanatomy: A brain structural argument for schizophrenia suggests that there are enlarged lateral ventricles (liquid filled cavities) in patients with schizophrenia compared those without schizophrenia. In addition, some research suggests schizophrenics have lower activity in the pre frontal cortex (which explains disordered and illogical thinking).
Immune system hyperactivity: in 2014, evidence emerged to support a recent theory that claims schizophrenia is caused by the brain’s immune functioning being hyperactive. Microglia, a type of cell which combats infection and ‘prunes’ unwanted synaptic connections, may be over-active and destroy the wrong connections in the brain, leaving it wired incorrectly. This causes the abnormal psychological experiences and functioning that is seen in schizophrenia. |
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A02 Other biological influences |
Immune system hyperactivity: while this is still a very new theory of schizophrenia, it offers an enormous possibility for advances in the diagnosis, prevention and treatment of schizophrenia. Brain inflammation due to over-active microglia can be detected by brain scans, so may lead to earlier diagnosis of schizophrenia. If the illness is detected early, outcomes are better in the long term. New treatments that target brain inflammation might also be helpful in preventing schizophrenia in those at risk, or treating it in those who already suffer from the illness. The theory is potentially very useful in advancing our understanding of schizophrenia and the range of options that can be offered to benefit patients. |
