Biological Explanations of Schizophrenia (AO1 + AO3)
The biological explanation focuses on genetics, dopamine function, and neural
correlates. Here's each component in detail:
1. Genetic Explanations (AO1)
Schizophrenia tends to run in families, suggesting a genetic basis. The closer the genetic
relatedness, the higher the risk:
• Gottesman (1991):
o MZ twins: 48% concordance
o DZ twins: 17%
o Siblings: 9%
Researchers have identified candidate genes involved in regulating dopamine and brain
development:
• Schizophrenia is polygenic (involves many genes) and aetiologically
heterogeneous (different combinations of genes in different people).
• Example: COMT and DISC1 genes have been linked to increased risk.
✅ AO3 Evaluation: Genetic Explanations
Strengths:
• Strong empirical support: Gottesman’s large twin study and adoption studies
(e.g., Tienari et al.) show a genetic link.
• Molecular genetic studies (e.g., Ripke et al., 2014) found 108 genetic variations
linked to schizophrenia, suggesting robust evidence.
Limitations:
, • Concordance is not 100% in MZ twins — suggests environmental factors (e.g.,
trauma, stress) must also play a role.
• Genetic evidence is correlational, not causal — it shows links, not mechanisms.
2. Dopamine Hypothesis (AO1)
This theory suggests abnormal dopamine activity causes schizophrenia.
Classic Dopamine Hypothesis:
• Schizophrenia is due to hyperdopaminergia (excess dopamine activity),
particularly in the subcortex (e.g., Broca’s area → auditory hallucinations).
Revised Dopamine Hypothesis:
• Hypodopaminergia in prefrontal cortex (too little dopamine) could explain
cognitive symptoms like disorganised thinking.
✅ AO3 Evaluation: Dopamine Hypothesis
Strengths:
• Supporting evidence from drug treatments:
o Antipsychotics block dopamine receptors → reduce symptoms.
o Dopamine agonists (e.g., amphetamines) induce psychotic symptoms in
healthy people.
• Imaging studies show increased dopamine synthesis in people with schizophrenia.
Limitations:
• Too simplistic: Doesn't account for all symptoms (e.g., negative symptoms may
not involve dopamine).
• Cause or effect?: Abnormal dopamine may be a result of schizophrenia, not the
cause.
• Ignores other neurotransmitters, e.g., glutamate.
The biological explanation focuses on genetics, dopamine function, and neural
correlates. Here's each component in detail:
1. Genetic Explanations (AO1)
Schizophrenia tends to run in families, suggesting a genetic basis. The closer the genetic
relatedness, the higher the risk:
• Gottesman (1991):
o MZ twins: 48% concordance
o DZ twins: 17%
o Siblings: 9%
Researchers have identified candidate genes involved in regulating dopamine and brain
development:
• Schizophrenia is polygenic (involves many genes) and aetiologically
heterogeneous (different combinations of genes in different people).
• Example: COMT and DISC1 genes have been linked to increased risk.
✅ AO3 Evaluation: Genetic Explanations
Strengths:
• Strong empirical support: Gottesman’s large twin study and adoption studies
(e.g., Tienari et al.) show a genetic link.
• Molecular genetic studies (e.g., Ripke et al., 2014) found 108 genetic variations
linked to schizophrenia, suggesting robust evidence.
Limitations:
, • Concordance is not 100% in MZ twins — suggests environmental factors (e.g.,
trauma, stress) must also play a role.
• Genetic evidence is correlational, not causal — it shows links, not mechanisms.
2. Dopamine Hypothesis (AO1)
This theory suggests abnormal dopamine activity causes schizophrenia.
Classic Dopamine Hypothesis:
• Schizophrenia is due to hyperdopaminergia (excess dopamine activity),
particularly in the subcortex (e.g., Broca’s area → auditory hallucinations).
Revised Dopamine Hypothesis:
• Hypodopaminergia in prefrontal cortex (too little dopamine) could explain
cognitive symptoms like disorganised thinking.
✅ AO3 Evaluation: Dopamine Hypothesis
Strengths:
• Supporting evidence from drug treatments:
o Antipsychotics block dopamine receptors → reduce symptoms.
o Dopamine agonists (e.g., amphetamines) induce psychotic symptoms in
healthy people.
• Imaging studies show increased dopamine synthesis in people with schizophrenia.
Limitations:
• Too simplistic: Doesn't account for all symptoms (e.g., negative symptoms may
not involve dopamine).
• Cause or effect?: Abnormal dopamine may be a result of schizophrenia, not the
cause.
• Ignores other neurotransmitters, e.g., glutamate.
