Schizophrenia-Biological Explanation Flashcards

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1
Q

Genetics -

A

Genes consist of DNA strands. DNA produces ‘instructions’ for general physical features of an organism (such as eye colour, height) and also specific physical features (such as neurotransmitter levels and size of brain structures). These may impact on psychological features (such as intelligence and mental disorder). Genes are transmitted from parents to offspring, i.e. inherited.

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2
Q

Dopamine -

A

A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson’s disease.

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3
Q

Dopamine -

A

A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson’s disease.

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4
Q

Neural correlates -

A

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.

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5
Q

Genetic Basis of Schizophrenia

A

Schizophrenia runs in families, suggesting a genetic link, although family members also share similar environments. Systematic studies show that greater genetic similarity between family members increases the likelihood of both developing schizophrenia.

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6
Q

What did Irving Gottesman’s (1991) study reveal about genetic similarity and schizophrenia?

A

Gottesman’s large-scale family study found a strong relationship between the degree of genetic similarity and the shared risk of schizophrenia.

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7
Q

Candidate Genes

A

Candidate genes are specific genes believed to increase the risk of inheriting schizophrenia. Schizophrenia is polygenic, meaning it involves multiple genes, and aetiologically heterogeneous, meaning different combinations of factors can lead to the condition.

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8
Q

What did Stephen Ripke et al. (2014) find in their genome-wide study on schizophrenia?

A

Ripke’s study analyzed the genetic data of 37,000 people with schizophrenia and 113,000 controls, identifying 108 genetic variations associated with increased risk, including genes involved in neurotransmitter function like dopamine.

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9
Q

Dopamine Hypothesis

A

Neurotransmitters, especially dopamine, are believed to function differently in the brain of a person with schizophrenia. Dopamine is essential in brain systems related to schizophrenia symptoms.

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10
Q

What role does dopamine play in schizophrenia?

A

Dopamine affects several brain areas involved in schizophrenia symptoms, with abnormalities in dopamine levels associated with different symptoms.

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11
Q

Hyperdopaminergia in the Subcortex

A

The original dopamine hypothesis focused on hyperdopaminergia, or high dopamine levels, in the subcortex. For example, excess dopamine receptors in Broca’s area may be linked to poverty of speech or auditory hallucinations.

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12
Q

How does hyperdopaminergia in Broca’s area relate to schizophrenia symptoms?

A

High dopamine levels in Broca’s area, which controls speech production, may contribute to symptoms like auditory hallucinations and reduced speech.

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13
Q

Hypodopaminergia in the Cortex

A

More recent dopamine hypotheses suggest hypodopaminergia, or low dopamine levels, in the cortex. Goldman-Rakic et al. (2004) linked low dopamine in the prefrontal cortex to negative symptoms.

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14
Q

What symptoms might result from hypodopaminergia in the prefrontal cortex?

A

Low dopamine levels in the prefrontal cortex, which controls decision-making and thinking, may cause negative symptoms like reduced motivation and impaired thought processes.

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15
Q

Combined Dopamine Hypothesis

A

It is possible that both hyperdopaminergia (high dopamine levels) in the subcortex and hypodopaminergia (low dopamine levels) in the cortex contribute to schizophrenia.

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16
Q

How might both high and low dopamine levels explain symptoms of schizophrenia?

A

High dopamine in certain brain areas may cause positive symptoms like hallucinations, while low dopamine in other regions may cause negative symptoms like lack of motivation.

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17
Q

Neural Correlates of Schizophrenia

A

Neural correlates are brain structures or functions that are associated with certain experiences, such as symptoms of schizophrenia. Both positive and negative symptoms have neural correlates.

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18
Q

What are neural correlates in schizophrenia?

A

They are measurements of brain structure or function that correlate with schizophrenia symptoms, helping researchers understand the brain’s role in these experiences.

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19
Q

Neural Correlates of Negative Symptoms (Avolition)

A

Avolition, a loss of motivation, involves the anticipation of reward. Abnormalities in the ventral striatum, which is involved in reward processing, may be linked to avolition.

20
Q

What did Juckel et al. (2006) find about activity levels in the ventral striatum in people with schizophrenia?

A

Juckel et al. found lower activity levels in the ventral striatum in schizophrenia patients, with a negative correlation between ventral striatum activity and the severity of negative symptoms.

21
Q

What did Juckel et al. (2006) find about activity levels in the ventral striatum in people with schizophrenia?

A

Juckel et al. found lower activity levels in the ventral striatum in schizophrenia patients, with a negative correlation between ventral striatum activity and the severity of negative symptoms.

22
Q

Neural Correlates of Positive Symptoms (Auditory Hallucinations)

A

Positive symptoms, such as auditory hallucinations, also have neural correlates. Allen et al. (2007) scanned the brains of people experiencing auditory hallucinations.

23
Q

What neural correlates did Allen et al. (2007) identify in people with auditory hallucinations?

A

They found lower activation in the superior temporal gyrus and anterior cingulate gyrus, with the hallucination group making more errors than controls, suggesting these brain areas are involved in auditory hallucinations.

24
Q

Genetic Susceptibility in Schizophrenia
Gottesman

A

There is substantial evidence from various sources supporting a genetic vulnerability to schizophrenia.

25
Q

What did Gottesman’s study reveal about genetic similarity and schizophrenia risk?

A

Gottesman’s study showed a strong correlation between genetic similarity and schizophrenia risk, indicating that genetic factors significantly increase vulnerability.

26
Q

Tienari et al. (2004) Adoption Study

A

Adoption studies by Tienari et al. (2004) showed that children of schizophrenia sufferers are at heightened risk of schizophrenia even if adopted into families without a history of the disorder.

27
Q

What does Tienari et al.’s study suggest about schizophrenia risk?

A

It suggests that genetic factors contribute to schizophrenia risk independently of family environment.

28
Q

Ripke et al. (2014) Molecular Level Study

A

Ripke et al. found that specific genetic variations at the molecular level significantly increase the risk of schizophrenia.

29
Q

How does Ripke et al.’s study support genetic susceptibility in schizophrenia?

A

It provides molecular evidence that certain genetic variations are associated with an increased risk of developing schizophrenia.

30
Q

Mixed Evidence for the Dopamine Hypothesis

A

There is mixed evidence supporting the dopamine hypothesis, which suggests abnormal dopamine functioning in schizophrenia.

31
Q

How do dopamine agonists and antipsychotic drugs provide evidence for dopamine’s role in schizophrenia?

A

Dopamine agonists increase dopamine levels, worsening symptoms, while antipsychotic drugs reduce dopamine activity, alleviating symptoms, suggesting dopamine involvement.

32
Q

Lindstroem et al. (1999) Radioactive Labelling Study

A

Lindstroem et al. (1999) used radioactive labelling to show that chemicals needed to produce dopamine are taken up faster in the brains of people with schizophrenia, suggesting higher dopamine production.

33
Q

What does Lindstroem et al.’s study suggest about dopamine levels in schizophrenia?

A

It indicates that people with schizophrenia may produce more dopamine than controls, supporting the dopamine hypothesis.

34
Q

Limitations of the Dopamine Hypothesis

A

While dopamine is a key factor, it does not fully explain schizophrenia. Genes identified in Ripke et al.’s study also code for other neurotransmitters, such as glutamate.

35
Q

What role does glutamate play in current schizophrenia research?

A

Glutamate is being investigated as an important neurotransmitter in schizophrenia, alongside dopamine, as suggested by research from Moghaddam and Javitt (2012).

36
Q

Correlation-Causation Problem in Neural Correlates

A

Neural correlates are brain abnormalities associated with symptoms of schizophrenia, but their existence does not prove causation.

37
Q

Why is there a correlation-causation issue in neural correlates of schizophrenia?

A

A correlation does not mean causation; abnormal brain activity might not cause symptoms directly and could result from or coexist with other factors.

38
Q

Example of Correlation-Causation in Ventral Striatum Activity

A

Lower activity in the ventral striatum correlates with negative symptoms, but it’s unclear if the activity reduction causes the symptoms or if the symptoms reduce activity.

39
Q

What alternative explanations exist for low ventral striatum activity in schizophrenia?

A

Reduced activity could be caused by negative symptoms themselves or by a third factor affecting both striatum activity and symptoms.

40
Q

The Role of Mutation

A

The Role of Mutation in Schizophrenia
Schizophrenia can occur even without a family history of the disorder.

41
Q

What is one explanation for cases of schizophrenia with no family history?

A

One explanation is DNA mutation in parental genes, especially in paternal sperm cells.

42
Q

Causes of DNA Mutation Leading to Schizophrenia

A

Mutations in parental DNA can be caused by factors like radiation, poison, or viral infection.

43
Q

What external factors can lead to DNA mutations that increase schizophrenia risk?

A

Radiation, poison, and viral infections can all lead to DNA mutations that may raise schizophrenia risk.

44
Q

Brown et al. (2002) Study on Paternal Age and Schizophrenia Risk

A

Brown et al. (2002) found a positive correlation between paternal age and schizophrenia risk.

45
Q

What did Brown et al. find about the relationship between paternal age and schizophrenia risk?

A

Schizophrenia risk increases with paternal age, from around 0.7% in fathers under 25 to over 2% in fathers over 50.

46
Q

Paternal Age and Risk of Schizophrenia

A

Older paternal age is associated with an increased risk of schizophrenia due to a higher likelihood of DNA mutations in sperm cells.

47
Q

How does paternal age affect schizophrenia risk?

A

As paternal age increases, the risk of sperm mutations rises, leading to a higher risk of schizophrenia in offspring.