Biological explanations of schizophrenia

genetic inheritance of schizophrenia

• Some people may have a genetic predisposition to schizophrenia, so the condition is at least partly inherited - runs in families through faulty genes.

• Schizophrenia is partly inherited. People who share more genes with a person with schizophrenia have a higher risk of developing it.

• Faulty gene - C4 gene involved in immune function and synaptic pruning

• individuals with increased C4 activity have a higher chance of developing SF

• Increased C4 activity is a genetic mutation

• C4 plays a role in pruning synapses / excessive pruning - symptoms seen in SF

• explains the thinner cerebral cortex of the SF patients - fewer synapses compared to healthy brains - accessory synaptic pruning during adolescence and early adulthood - due to increased C4 activity - cognitive symptoms seen in schizophrenia

• Family studies

  • Risk increases the more genes you share with someone with schizophrenia

research - Gottesman and shield:

• children of 2 SF patients who share 100 % genetic similarity have a 46% chance of developing the disorder.

• Monozygotic twins who share 100% genetic similarity have a 48% chance of developing the disorder if one twin has been diagnosed.

• First-degree relatives (children) who share 50% DNA with sufferer have a 13% chance of developing the disorder if a parent has been diagnosed.

• Second-degree relatives (grandchildren) share 25% genetic similarity and have a 5 percent chance of developing SF if a grandparent has been diagnosed

Twin studies

• MZ (identical) twins share 100% genes → higher concordance

• DZ (non-identical) twins share 50% → lower concordance

• Gottesman (1991):

  • MZ: 48%

  • DZ: 17%

• General population: 1%

• Sibling: ~9%

• Parent: ~6%

• Both parents: ~46%

research adoption studies:

Joseph - genetic similarity can increase risks of developing the condition - found 40% concordance rate in schizophrenia for MZ twins (share 100% genetic similarity)

7% concordance rate for DZ twins ( share 50% genetic similarity) 

higher concordance rate for MZ twins - not due to environmental influence but genetic ( both MZ and DZ same environment but MZ higher CR)

suggests genes have some influence on the development of the disorder

Tienari - genetic influence in schizophrenia

• completed an adoption study in Finland with over 164 adopted kids whose biological mothers had been diagnosed with schizophrenia

• These were matched with kids whose biological mothers did not suffer from schizophrenia

• A study found that 11 of the sample whose biological mothers had schizophrenia had also been diagnosed with the condition, compared to just 4 from the control group ( non non-schizophrenic mothers)

• conclusion - schizophrenia has a genetic component, as the adopted children do not share environmental influences with their biological mothers.

• if the biological mother had a history of schizophrenia, the adopted child had a 10% chance of developing it too

• if not, then the rate remained 1% ( normal rate for the population)

• Candidate genes :

• Schizophrenia is polygenic: many genes increase risk

• Also aetiologically heterogeneous: different gene combinations in different people

• COMT, DISC1, and others linked to neurotransmitter regulation (dopamine, glutamate)

evaluation for the genetic influence of schizophrenia

✔ Strengths

P: A major strength of the genetic explanation is the strong research support showing a link between genetic similarity and schizophrenia risk.
E: For example, Gottesman found that the concordance rate for schizophrenia was 48% in monozygotic (MZ) twins but only 17% in dizygotic (DZ) twins, showing that the greater the genetic similarity, the higher the risk. Adoption studies also support this: Tienari et al. found that adoptees with a biological parent with schizophrenia were significantly more likely to develop the disorder than those with no genetic risk.
E: These findings suggest that genetic factors play a major role because biological relatedness strongly predicts vulnerability.
L: Therefore, consistent research evidence increases the validity of the genetic explanation for schizophrenia.

P: A further strength is that genetic research has led to useful real-world applications.
E: If schizophrenia risk is partly inherited, individuals with a strong family history can be identified as having higher vulnerability. This allows for genetic counselling, early monitoring, and early psychological or family-based interventions.
E: As a result, people who are genetically at-risk may receive support before symptoms become severe, potentially reducing long-term negative outcomes.
L: This practical usefulness of genetic research increases its value and supports the importance of genetic explanations.

✘ Weakness

P: A limitation is that genetic explanations are incomplete because they overlook important psychological and cognitive factors.
E: Cognitive explanations, such as dysfunctional information processing or faulty attentional systems, have strong empirical support and help explain symptoms like hallucinations and delusions. Psychological trauma and family dysfunction also offer alternative explanations.
E: This means that focusing only on genes does not provide a full understanding of the disorder and ignores other key influences.
L: Therefore, genetic explanations lack explanatory breadth and must be combined with psychological accounts for a more complete understanding.

P: The genetic explanation is also criticised for being biologically reductionist.
E: It reduces a complex mental disorder to genes and inherited vulnerability, ignoring social, emotional, environmental, and cognitive factors.
E: Schizophrenia involves a wide range of interacting influences, and a purely genetic account oversimplifies this complexity.
L: Therefore, while genetics plays a role, a reductionist approach limits the explanation’s overall validity.

P: Another limitation is that concordance rates in MZ twins are far below 100%, even though they share 100% of their genes.
E: Gottesman found the concordance rate for MZ twins to be around 48%, meaning over half of genetically identical twins do not both develop schizophrenia.
E: This clearly shows that environmental triggers, stress, family interactions, or life events must play a major role because genes alone cannot fully account for the disorder.
L: This supports the interactionist approach (diathesis–stress model) rather than a purely genetic explanation.

The dopamine hypothesis

• Symptoms of schizophrenia are caused by abnormal dopamine activity.

• The biochemical explanation of SF argues that it’s caused by elevated levels of dopamine at key synaptic sites within subcortical regions of the brain (mesolimbic pathway and limbic system

• The excess of dopamine is argued to cause a ‘ system overload.’

• too many impulses are being transmitted ( too much happening)

• triggers positive symptoms of schizophrenia ( delusions)

• can be caused by presynaptic neurons releasing too much dopamine

• at a postsynaptic level, there may not be enough dopamine being broken down after synaptic transmission

• leaving too much dopamine in the surrounding cells

• reuptake processes may be impaired leaving too much dopamine in the synapse,

• abnormalities in dopamine can manifest in odd behavioural patterns found in some schizophrenic patients ( creating visual hallucinations)

• D2 receptors ( HYPODAPERMINERGIA) - SF are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and so more neurons tiring.

• Theory claims that excessive amounts of dopamine or an oversensitivity of the brain to dopamine leads to positive symptoms of schizophrenia

• evidence from drugs: antipsychotic drugs - dopamine antagonists - block the activity of dopamine in the brain by reducing the stimulation of the dopamine hypothesis - eliminates hallucinations and delusions

• by alleviating many of the symptoms of schizophrenia, antipsychotic drugs strengthen the case for dopamine being a significant contributory factor.

• Revised dopamine hypothesis:

• Positive symptoms = too much dopamine in certain pathways

• Negative symptoms = too little dopamine in the cortex (especially the prefrontal cortex)

• Davis et al - pointed out that in the prefrontal cortex, there are no D2 receptors, and actually, there appears to be a deficiency of dopamine in this region

• suggests that low levels of dopamine in this region ( meso cortical pathway) are more responsible for negative symptoms of schizophrenia, like avolition. This is called Hypo-dopaminergia 

• negative symptoms of schizophrenia ( avolition) can also be explained by lower levels of dopamine in the prefrontal cortex, where there is no D2 receptors - Hypodopaminergia

• amphetamines: dopamine agonist stimulates nerve cells containing dopamine, causing synapses to be flooded - large doses of the drug can cause hallucinations and delusions of a schizophrenic episode.

dopamine hypothesis - dopamine pathways

• mesolimbic pathway - overactive dopamine transmission - associated with positive symptoms: hallucinations, delusions and thought disorder.

• mesocortical pathway - underactive dopamine transmission - associated with negative symptoms: avolition, social withdrawal and flat affect

• mesocortical pathway - also linked to cognitive symptoms : poor attention , impaired planning.

research for dopamine hypothesis

• randrup Munkdav:

• aim - to investigate the effects of increased dopamine levels on behaviour

• procedure - they gave amphetamine (a stimulant drug that increases dopamine release to animals such as rats and monkeys ) 

• also tested whether antipsychotic drugs, which block dopamine receptors, could reverse these changes

• findings - the animals began showing stereotyped, repetitive behaviours ( pacing, head movements) and became agitated and hyperactive 

• at high doses amphetamines can also cause psychosis like symptoms in humans (hallucinations and paranoia)

• when antipsychotics drugs were given these abnormal behaviours decreased

• conclusions - excess dopamine activity leads to behaviours similar to the positive symptoms of schizophrenia 

• reducing dopamine activity ( antipsychotics ) reduces these behaviours

• dopamine overactivity is linked to schizophrenias.

Revised Dopamine Hypothesis (Hypodopaminergia + Pathways)

The revised dopamine hypothesis suggests that schizophrenia is caused by both increases and decreases in dopamine activity in different areas of the brain, rather than simply “too much dopamine overall”.

Positive symptoms = Hyperdopaminergia (too much dopamine)

Positive symptoms (hallucinations, delusions) are linked to excess dopamine in specific pathways:

• Mesolimbic pathway
  This pathway runs from the ventral tegmental area (VTA) to the nucleus accumbens.
  Too much dopamine here is believed to cause positive symptoms, such as hallucinations, delusions, and feelings of abnormal salience (giving too much meaning to irrelevant stimuli).

Negative and cognitive symptoms = Hypodopaminergia (too little dopamine)

The revised model proposes that low dopamine in some regions also contributes to schizophrenia:

• Mesocortical pathway
  This pathway goes from the VTA to the prefrontal cortex, an area involved in executive functioning.
  Low dopamine here (hypodopaminergia) is associated with:

  • Negative symptoms (avolition, flat affect)

  • Cognitive deficits (poor working memory, attention problems)

How the revised hypothesis works together

The key idea is that schizophrenia involves a dopamine imbalance, not simply an overall excess:

• Too much dopamine in the mesolimbic pathway → positive symptoms

• Too little dopamine in the mesocortical pathway → negative & cognitive symptoms

This explains why the disorder has such a wide range of symptoms, and why treatments that reduce dopamine help with positive symptoms but do not always fully eliminate negative symptoms.

evaluation for dopamine hypothesis theory

✔ Strengths

P: One strength of the dopamine hypothesis is strong supporting evidence from controlled animal studies.
E: Randrup and Munkvad found that injecting rats with amphetamines, which increase dopamine activity, produced schizophrenia-like behaviours such as agitation and stereotyped movements.
E: When the dopamine levels were later reduced using neuroleptic drugs, these behaviours decreased, supporting the idea that excess dopamine can cause psychotic symptoms.
L: This research increases the credibility of the dopamine hypothesis by showing a clear link between dopamine activity and schizophrenia-like symptoms.

P: Another strength is that the dopamine hypothesis has led to highly effective real-world treatments.
E: Antipsychotic medications, such as chlorpromazine and atypical drugs, work by blocking dopamine receptors and reducing dopamine activity in key brain pathways.
E: These drugs successfully reduce positive symptoms such as hallucinations and delusions for the majority of patients, showing that dopamine plays a significant role in symptom production.
L: The effectiveness of antipsychotics supports the validity of the dopamine hypothesis and highlights its practical usefulness.

P: A further strength is that the dopamine hypothesis becomes more complete when integrated into an interactionist framework.
E: The diathesis–stress model suggests that genetic vulnerability (such as abnormal dopamine functioning) interacts with environmental stressors to trigger schizophrenia.
E: This combined explanation recognises the role of dopamine while also accounting for environmental influences like trauma, drug use, or family stress.
L: Therefore, linking dopamine with the diathesis–stress model offers a more holistic and realistic explanation of schizophrenia’s development.

✘ Limitations

P: A limitation of the dopamine hypothesis is that much of the evidence struggles with cause and effect.
E: Findings often show that people with schizophrenia have increased dopamine activity, but this does not prove that dopamine abnormalities cause the disorder.
E: It is possible that dopamine dysfunction is a result of schizophrenia or even an effect of taking antipsychotic medication, meaning the direction of causality is unclear.
L: This weakens the hypothesis because it cannot confidently state that dopamine overactivity is the origin of the disorder.

P: Another weakness is that the dopamine hypothesis may demonstrate beta bias.
E: Much early research into dopamine and schizophrenia—especially animal studies and drug trials—was conducted mainly on male participants or male animals, assuming findings would apply equally to both sexes.
E: This is problematic because males and females may have different hormonal interactions with dopamine systems, meaning the theory may not fully represent female experiences of schizophrenia.
L: As a result, the dopamine hypothesis may lack population validity due to gender-biased assumptions.

Neural correlates of schizophrenia ( structure or brain and biochemistry)

• schizophrenia is a result of further abnormalities in the structure of the brain

Enlarged ventricles:

• People with schizophrenia often have enlarged ventricles, which are fluid-filled spaces in the brain.

• In schizophrenic patients, ventricles are typically about 15% larger than normal.

• Enlarged ventricles indicate loss or shrinkage of brain tissue, and research shows schizophrenic brains tend to be lighter due to reduced grey matter.

• This grey matter loss is linked to cognitive impairment and negative symptoms, such as avolition and poor executive functioning.

• It is unclear whether enlarged ventricles are a cause or an effect of schizophrenia, but the correlation is strong.

• This pattern of grey matter reduction is consistent with the typical onset of schizophrenia in late adolescence or early adulthood.

ventral striatum:

What is the ventral striatum?

• A brain region involved in:

  • Reward processing

  • Motivation

  • Feeling pleasure

• Strongly connected to the dopamine system

UNDERACTIVITY → Negative Symptoms Key idea

In schizophrenia, the ventral striatum often shows underactivity (reduced activity).

Why this matters

If the ventral striatum doesn't respond properly to rewards, the person doesn’t feel motivated or excited by things.

This leads to negative symptoms such as:

• Apathy (not caring about doing anything)

• Avolition (lack of motivation)

• Anhedonia (reduced pleasure)

OVERACTIVITY → Positive Symptoms Key idea

Some research suggests that, due to dysregulated dopamine, the ventral striatum and related dopamine pathways can also become overactive.

Why this matters

Too much dopamine causes the brain to:

• Assign too much importance (“abnormal salience”) to things

• Misinterpret internal thoughts as real

• Pay attention to irrelevant stimuli

This can produce positive symptoms.

Leads to positive symptoms such as:

• Hallucinations

• Delusions

Superior temporal gyrus and anterior cingulate gyrus:

What is the Superior Temporal Gyrus (STG)?

• A brain region involved in auditory processing and language comprehension.

• Helps the brain interpret sound and understand speech.

Role in schizophrenia

• In schizophrenia, the STG is often underactive or has abnormal functioning.

• There are disrupted connections between the STG and other regions, especially the prefrontal cortex and speech production areas.

Why this causes auditory hallucinations

Normally, the brain knows when a voice or thought comes from inside yourself.

But in schizophrenia:

The STG does not correctly process inner speech.

• As a result, internal thoughts can be misinterpreted as external voices.

• This leads to auditory hallucinations, a key positive symptom.

What is the Anterior Cingulate Gyrus (ACG)?

• A region involved in:

  • Monitoring conflicts in thinking

  • Distinguishing self-generated actions from external events

  • Attention and emotional regulation

Role in schizophrenia

• In schizophrenia, the ACG often shows abnormal activation.

• This reduces the brain’s ability to label inner speech as “self-generated.”

Why this matters

If the ACG cannot recognise a thought as your own:

• The brain incorrectly concludes it must come from someone else.

• This further contributes to auditory hallucinations and delusional beliefs.

hypo frontality:

What is Hypofrontality?

• Hypofrontality refers to reduced activity and decreased cerebral blood flow in the prefrontal cortex.

• The prefrontal cortex is involved in:

  • Planning

  • Decision-making

  • Concentration

  • Problem solving

  • Regulating emotions

Hypo frontality in Schizophrenia

Research shows that people with schizophrenia often show:

• Lower levels of blood flow and metabolic activity in the prefrontal cortex

• Reduced size/volume of certain connected brain regions such as the hippocampus and amygdala

This contributes to:

• Cognitive impairments (poor attention, disorganised thinking, poor working memory)

• Negative symptoms, especially flat affect (reduced emotional expression)

Hippocampus and Amygdala (volume reduction → emotional disruption)

Hippocampus

• Important for memory and linking emotions to experiences.

• In schizophrenia, the hippocampus is often smaller or shows reduced volume.

• This contributes to memory problems and difficulty forming coherent thoughts

Amygdala

• Important for processing emotion, fear, and social responses.

• In schizophrenia, the amygdala also tends to be smaller or underactive.

• This leads to:

  • Dulled emotional responses

  • Flat affect (lack of facial expression or emotional display)

research for neural explanations for schizophrenia

• Torrey:

• reviewed brain scans of people with schizophrenia

• found that people with schizophrenia have enlarged lateral and third ventricles

• enlarged ventricles indicate loss of brain tissue, especially in the frontal and temporal lobes

• frontal , temporal - important for thinking , emotion , decision making

• supports neural explanation - showing schizophrenia is linked to physical brain abnormalities

McEwen:

• studied the effects of chronic stress on the brain, on neurons in the hippocampus and prefrontal cortex

• Chronic stress can cause the shrinkage of neurons and loss of synapses in the hippocampus and prefrontal cortex

• These changes affect cognition, emotion, and memory

• Stress interacts with vulnerable brain structures, which may trigger or worsen schizophrenia

• shows that environmental factors (stress can affect neural structure, linking to the diathesis stress model of schizophrenia

• supports biological explanation - schizophrenia involves neural changes, not just psychological symptoms.

evaluation for neural explanations for schizophrenia

✔ Strengths

P: One strength of neural explanations is that they simplify the causes of schizophrenia into clear, measurable brain abnormalities.
E: For example, focusing on neuroanatomical issues such as hypofrontality in the prefrontal cortex gives clinicians a direct biological target to treat.
E: This is far easier to address through medical or neurological interventions than more complex and multifaceted explanations such as dysfunctional family environments, which are harder to define and treat.
L: Therefore, neural explanations have practical value because they offer specific biological targets for treatment, increasing their usefulness in real-world clinical practice.

P: Another strength is the strong research support for neural explanations.
E: Torrey found that individuals with schizophrenia often have enlarged ventricles, which indicates a loss of brain tissue in key areas such as the frontal and temporal lobes.
E: This clear biological difference between schizophrenic and non-schizophrenic brains supports the idea that structural abnormalities are linked to the disorder.
L: Such objective scientific findings increase the validity of neural explanations for schizophrenia.

P: A further strength is that similar neural abnormalities are found in other mental disorders, which supports the scientific credibility of neural explanations.
E: For instance, Parkinson’s disease also involves dopamine dysfunction, showing that biological mechanisms can reliably explain a range of disorders.
E: This strengthens psychology as a science because it demonstrates that mental disorders can be studied using objective, measurable biological tools, such as brain scans and neuroimaging.
L: Therefore, neural explanations help establish psychology as a scientific discipline through their reliance on valid, empirical methods.

✘ Limitations

P: A key limitation of neural explanations is that most of the evidence is correlational, meaning it shows an association but not causation.
E: For example, studies find that people with schizophrenia often have enlarged ventricles or reduced prefrontal cortex activity, but it is unclear whether these brain differences cause schizophrenia or are a result of the disorder.
E: This makes it difficult to determine whether neural abnormalities are the origin of the disorder or a consequence of living with schizophrenia, including the effects of medication or lifestyle factors.
L: Therefore, neural explanations are limited in explanatory power because they cannot confidently establish a direct causal relationship between brain structure/function and schizophrenia.

P: Neural explanations are biologically reductionist, meaning they reduce a complex disorder to brain structures or neurotransmitters alone.
E: Schizophrenia also involves psychological and social factors, such as trauma, stress, and family dysfunction, which neural explanations often ignore.
E: By focusing only on measurable brain abnormalities, these explanations oversimplify the disorder and fail to account for the multifaceted nature of schizophrenia.
L: This limits the explanation’s overall validity, as it cannot fully explain why some people with brain abnormalities do not develop schizophrenia.

P: Another limitation is the problem of cause and effect in neural explanations.
E: For example, hypofrontality or enlarged ventricles are often observed in people with schizophrenia, but it is unclear whether these abnormalities predate the disorder or are consequences of having schizophrenia, such as stress, medication, or lifestyle factors.
E: This makes it difficult to claim that neural correlates are the direct cause of symptoms.
L: Therefore, neural explanations struggle to establish causal relationships, reducing their explanatory power.