Schizophrenia Biological Explaination Flashcards
(10 cards)
What is the genetic explanation of schizophrenia?
Schizophrenia is polygenic—multiple genes increase risk. Genes code for biological processes affecting brain structure and neurotransmission.
What evidence supports the genetic explanation?
Concordance rates are higher in relatives—1% in general population, 17% in DZ twins, 48% in MZ twins—indicating genetic influence.
What are neural correlates in schizophrenia?
Neural correlates are brain structure or function abnormalities linked to symptoms, e.g., enlarged ventricles and activity changes in the striatum or Broca’s area.
What is the dopamine hypothesis?
Schizophrenia symptoms are linked to dopamine imbalance: excess dopamine (hyperdopaminergia) in Broca’s area causes hallucinations; low dopamine (hypodopaminergia) in the prefrontal cortex causes negative symptoms.
What role does glutamate play in schizophrenia?
Glutamate levels are reduced in schizophrenia. As an excitatory neurotransmitter, it’s linked to attention, memory, and learning deficits.
What structural brain abnormality is linked to schizophrenia?
Enlarged ventricles—fluid-filled brain cavities—are associated with tissue loss and are commonly found in schizophrenia patients.
AO3 – Strength: Strong evidence for genetic vulnerability (Gottesman, Tienari, Ripke)
A strength of the genetic explanation is strong supporting evidence. Gottesman (1991) found schizophrenia concordance rates of 48% for MZ twins and 17% for DZ twins, showing higher genetic similarity increases shared risk. Tienari et al. (2004) found 6.7% of adoptees with schizophrenic biological mothers developed schizophrenia, compared to just 2% with non-schizophrenic mothers, despite being raised in healthy adoptive homes. Ripke et al. (2014), in a genome-wide study of 37,000 patients, identified 108 genetic variations linked to increased risk. This robust evidence shows genetic vulnerability plays a significant role, even if schizophrenia isn’t entirely genetic.
AO3 – Limitation: Mixed evidence for the dopamine hypothesis (Curran, Tauscher, Lindstroem, Moghaddam)
A limitation of the dopamine hypothesis is that the evidence is mixed. Curran et al. (2004) found dopamine agonists like amphetamines worsen symptoms and can cause psychosis in non-sufferers, while Tauscher et al. (2014) showed antipsychotics reduce dopamine and alleviate symptoms. Lindstroem et al. (1999) used radioactive labelling to show faster uptake of L-DOPA in schizophrenia patients, suggesting overactive dopamine production. However, Ripke et al. (2014) found genes linked to other neurotransmitters too, and Moghaddam & Javitt (2012) highlighted glutamate dysfunction. This shows dopamine plays a role, but is not the whole explanation.
AO3 – Limitation: Correlation-causation problem in neural correlates
A key issue with neural correlates is the correlation-causation problem. Reduced activity in the ventral striatum is linked to negative symptoms like avolition, while increased activity in Broca’s area is linked to auditory hallucinations. However, this doesn’t prove causality—it’s unclear whether brain abnormalities cause the symptoms, or if the symptoms cause brain changes. Alternatively, a third factor may influence both. Neural correlates highlight brain areas involved but don’t explain how or why schizophrenia develops, limiting their explanatory value.
AO3 – Limitation: Biological reductionism and ignoring environmental factors
A limitation of the biological explanation is that it ignores environmental and psychological factors. MZ twins show only 48% concordance, suggesting genes are not the sole cause. Family dysfunction, childhood trauma, or high expressed emotion may also contribute. This supports the diathesis-stress model, which argues schizophrenia results from genetic vulnerability plus environmental triggers. A purely biological view is therefore reductionist and cannot fully explain the complexity of the disorder.
