Family studies find individuals with schizophrenia and determine whether their biological relatives are similarly affected more often than non-relatatives.
Family studies have established that schizophrenia is more common amoung biological relatives of the person with schizophrenia - the closer the degree of genetic relatedness, the greater the risk.
Gottesman (1991) found that someone with an aunt with schizophrenia has a 2% chance of developing it, increasing to 9% if the individual is a sibling, and 48% if they are an identical twin.
Research has shown thet schizophrenia is polygenic which means that a number of diffrent genes are involved. The most likely ones are those coding for neurotransmitters like dopamine.
Ripke et al studied the genetic makeup of 37,000 people with schizophrenia and compaired them to 113,000 controls. They identified 108 genetic variations, each slightly increasing the risk of schizophrenia.
Schizophrenia is aetiologically heterogenous - different combinations can lead to it.
Schizophrenia can also have a genetic origin in the absence of family history of the disorder. This could be because of a mutation in parentalDNA due to; radiation, poison, viralinfection ect.
Brown et al (2002) found a positive correlation between paternal age and risk of schizophrenia - older males associated with sperm mutation. Increased risk for those >25 have a 0.7% risk while those <50 have a 2% risk.
Neural Correlated - Patterns of structure or activity in the brain that occur in conjunction with experience and may be implicated in the origins of that experience.
The dopamine hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with positive symptoms of schizophrenia.
Excess DA receptors in pathways from the subcortex to Broca's aera may explain specific symptoms of schizophrenia such as auditory hallucinations.
Dopamine hypothesis suggests that schizophrenics are through to have abnormally high numbers of DA receptors on recieving neurones, resulting in more dopamine binding and therefore more neurones firing.
There are two sources of evidence for the role of dopamine in schizophrenia. These are Drugs that increase and decrease dopaminergic activity.
Drugs that increase dopaminergic activity - Amphetamine is a dopamine agonist, i.e. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter.
Drugs that decrease dopaminergic activity - Although there are many different types of antipsychotic drugs, they all have one thing in common; they block the activity of dopamine in the brain. These drugs are known to eliminate symptoms such as hallucinations and delusions.
The revised dopamine hypothesis - Davis et al
Proposed that positive symptoms are caused by excessive dopamine in the subcortical areas of the brain.
The negative symptoms for schizophrenia, are thought to arise from a deficit of dopamine in areas of the prefrontal cortex.
Patel at al found lower levels of dopamine in the prefrontal cortex of schizophrenia patients compaired to their control group.
Evaulation of Genetic Factors - Supporting Argument
Gottesman shows how genetically similarity and shared risk of schizophrenia is related.
Tienari et al (2004) shows children of schizophrenix are still at heightened risk of schizophrenia if adopted into families with no history of the condition.
Hilker et al (2008) showed a concordance rate of 33% in twins.
Evaluation of Genetic Factors - Biological Reductionism
Reseach has shown that environmental factors can also increase the chance of developing schizophrenia. This includes risk factors during birth and smoking of THC-richcannabis in teenage years.
Psychological risks could include childhoodtrauma which leads people to be more vulnerable to adult mentalhealth problems.
Evaluation of Neural Correlates - Evidence from treatment
Leuchet et al carried out a meta analysis of 212 studies. They concluded that all the antipsychotic drugs testing in studies were significantly more effective than placebos in the treatment of positive and negative symptoms, achieved by reducing the effects of dopamine.
Evaluation Neural Correlates - Glutamate
Post-mortem and live scanning studies have consistently founf raised levels of the neurotransmitter glutamate in serval brain regions of people with schizophrenia
In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing