biological explanations for schizophrenia

• Genetics ?

  Genes consist of DNA strands. DNA produces 'instructions' for general physical features of an organism and also specific physical features. may impact on psychological features. Genes are transmitted from parents to offspring, i.e. inherited.
• Neural correlates ?

  Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.
• Dopamine ?

  neurotransmitter that generally has an excitatory effect and is linked to the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson's disease.
• Family studies?

  confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder. For example (Gottesman study) 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 identical twin. family members tend to share aspects of their environment as well as many of their genes, so the correlation represents both - but family studies still give good support for the importance of genes in schizophrenia.
• Candidate genes ?

  number of diff genes involved, i.e. polygenic. most likely genes are those coding for neurotransmitters like dopamine. Ripke et al. combined previous data from genome-wide studies of schizophrenia. genetic make-up of 37,000 people with schizophrenia compared to 113,000 controls, 108 separate genetic variations associated with increased risk of schizophrenia. as diff studies identified diff candidate genes, schizophrenia is aetiologically heterogeneous, i.e. diff combos of factors, lead to condition.
• The role of mutation ?

  Schizophrenia can have a genetic origin in the absence of a family history of the disorder. One explanation for this is mutation in parental DNA which caused by radiation, poison or viral infection.

  Evidence for mutation comes from positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al. 2002)
• The original dopamine hypothesis ?

  original hypothesis based on discovery that drugs used to treat schizophrenia caused symptoms similar to those in people with Parkinson's disease, condition associated with low DA levels. so schizophrenia might be result of high levels of DA (hyperdopaminergia) in subcortical areas of the brain. For example, an excess of DA receptors in pathways from the subcortex to Broca's area (responsible for speech production) may explain specific symptoms of schizophrenia such as poverty of speech and/or auditory hallucinations.
• Updated versions of the dopamine hypothesis ?

  Davis et al. proposed addition of cortical hypodopaminergia. can explain symptoms of SZ. e.g. low DA in prefrontal cortex explains cognitive problems. said that cortical hypodopaminergia leads to subcortical hyperdopaminergia- so both high & low levels of DA in diff brain regions part of updated version. current versions of dopamine hypothesis try explain origins of abnormal DA function. So both genetic variations and early experiences of stress, make some people more sensitive to cortical hypoD & so subcortical hyperD
• one strength of the genetic explanation?

  P - strong evidence base.

  E - Family studies such as gottesman show that risk increases with genetic similarity to a family member with schizophrenia studies such as tienari et al show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family. A recent twin study by Hilker et al. showed a concordance rate of 33% for identical twins and 7% for non-identical twins.

  L - some people are more vulnerable to schizophrenia as a result of their genetic make-up.
• One limitation of the genetic explanation?

  P - clear evidence to show that environmental factors also increase the risk of developing schizophrenia.

  E - These environmental factors include both biological and psychological influences. Biological risk factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia. In one study by Merkved et al. (2017), 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.

  L - genetic factors alone cannot provide a complete explanation for schizophrenia.
• One strength for neural correlates in schizpophrenia?

  P - support for the idea that dopamine (DA) is involved in schizophrenia.

  E - amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without. also antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms. lastly, some candidate genes act on the production of DA or DA receptors.

  L - strongly suggests that dopamine is involved in the symptoms of schizophrenia.
• One limitation of the dopamine hypothesis ?

  P - evidence for a central role of glutamate.

  E - Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia. In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.

  L - equally strong case can be made for a role for other neurotransmitters.