SCHIZOPHRENIA
Genetic Basis
Gottesman did a 1991 large scale family study and found a strong positive correlation
between genetic similarity and shared risk of schizophrenia.
Joseph (2004) calculated the pooled data for all schizophrenia data prior to 2001 and
found a concordance rate of 40.4% for MZ twins and 7.4% for DZ twins.
Adoption studies
Tienari et al. (2000) did a study of 164 adoptees who had biological mothers who
were diagnosed with schizophrenia and 197 who weren’t, and 6.7%/11 of those with
schizophrenia mothers got diagnosed with it, compared to 2%/4 of the control group.
Candidate genes
There have been genes which have been associated with a higher risk of
schizophrenia, Stephen Ripke et al. (2014) compared 37,000 patients with 113,000
controls and 108 genetic variations were associated with a high risk of schizophrenia.
Evaluation
+ Research support, Ripke, Tiernari, Gottesman and Joseph.
+ Genetic mutation can cause schizophrenia, Brown et al. (2002) found a
positive correlation between paternal age (which is associated with a higher
risk of sperm mutation) and risk of schizophrenia.
- Research has shown that a negative emotional climate that someone can’t
cope with can trigger a schizophrenic episode.
, -
SCHIZOPHRENIA
The probability of developing schizophrenia for identical twins is less than
50% so perhaps emotional triggers are important in the development of
schizophrenia.
- Twins grow up in a similar environment meaning that it can play a factor in
developing schizophrenia, Joseph (2004) points out that MZ twins are treated
as ‘twins’ (causing ‘identity confusion’) and not individuals unlike DZ twins, so
the difference in concordance rates could be due to environmental factors
that distinguishes the two types of twin.
The Dopamine Hypothesis
, SCHIZOPHRENIA
Neurotransmitters
Dopamine is excitatory,with a sensation of pleasure and its abnormal functioning is
linked to schizophrenia, especially high levels and the positive symptoms of
schizophrenia.
Schizophrenics are thought to have an abnormally high amount of D2 receptors
which causes more dopamine binding, leading to more firing neurons, leading to
positive symptoms.
It was found that people exposed to large doses of dopamine releasing drugs like
amphetamine caused ‘normal’ individuals to experience hallucinations and delusions
characteristic of schizophrenia.Grilly also found that when people with PArkinsons
(characterised by low dopamine levels) were given the drug L-dopa which raises
dopamine levels they’d develop schizophrenic like symptoms.
It was found that antipsychotic drugs all blocked dopamine activity and the fact that
they alleviate symptoms like hallucinations and delusions shows us that dopamine
does have a role in schizophrenia.
Hyperdopaminergia in the Subcortex
This focuses on high levels of dopamine in the subcortex, for example, an excess of
dopamine receptors in Broca’s area (the area responsible for speech production)
could be associated with speech poverty and/or auditory hallucinations.
Hypodopaminergic in the Cortex
This focuses on abnormal dopamine systems in the brain’s cortex.Goldman-Rakic et
al.(2004) has found a role in how low levels of dopamine in the prefrontal cortex
(responsible for decision making and thinking) are responsible for the negative
symptoms of schizophrenia.
Neural Correlates of Schizophrenia
Neural correlated = Measurements of the structure or function of the brain that
correlates with an experience and may be implicated as the cause.
Neural Correlates of Negative Symptoms
Juckel et al. found abnormally lower activity in the ventral striatum (responsible for
the anticipation of a reward) in schizophrenics (this may be the cause of avolition
(loss of motivation) compared to controls and found a negative correlation between
its activity and the severity of overall negative symptoms of schizophrenia.
Neural Correlates of Positive Symptoms
Genetic Basis
Gottesman did a 1991 large scale family study and found a strong positive correlation
between genetic similarity and shared risk of schizophrenia.
Joseph (2004) calculated the pooled data for all schizophrenia data prior to 2001 and
found a concordance rate of 40.4% for MZ twins and 7.4% for DZ twins.
Adoption studies
Tienari et al. (2000) did a study of 164 adoptees who had biological mothers who
were diagnosed with schizophrenia and 197 who weren’t, and 6.7%/11 of those with
schizophrenia mothers got diagnosed with it, compared to 2%/4 of the control group.
Candidate genes
There have been genes which have been associated with a higher risk of
schizophrenia, Stephen Ripke et al. (2014) compared 37,000 patients with 113,000
controls and 108 genetic variations were associated with a high risk of schizophrenia.
Evaluation
+ Research support, Ripke, Tiernari, Gottesman and Joseph.
+ Genetic mutation can cause schizophrenia, Brown et al. (2002) found a
positive correlation between paternal age (which is associated with a higher
risk of sperm mutation) and risk of schizophrenia.
- Research has shown that a negative emotional climate that someone can’t
cope with can trigger a schizophrenic episode.
, -
SCHIZOPHRENIA
The probability of developing schizophrenia for identical twins is less than
50% so perhaps emotional triggers are important in the development of
schizophrenia.
- Twins grow up in a similar environment meaning that it can play a factor in
developing schizophrenia, Joseph (2004) points out that MZ twins are treated
as ‘twins’ (causing ‘identity confusion’) and not individuals unlike DZ twins, so
the difference in concordance rates could be due to environmental factors
that distinguishes the two types of twin.
The Dopamine Hypothesis
, SCHIZOPHRENIA
Neurotransmitters
Dopamine is excitatory,with a sensation of pleasure and its abnormal functioning is
linked to schizophrenia, especially high levels and the positive symptoms of
schizophrenia.
Schizophrenics are thought to have an abnormally high amount of D2 receptors
which causes more dopamine binding, leading to more firing neurons, leading to
positive symptoms.
It was found that people exposed to large doses of dopamine releasing drugs like
amphetamine caused ‘normal’ individuals to experience hallucinations and delusions
characteristic of schizophrenia.Grilly also found that when people with PArkinsons
(characterised by low dopamine levels) were given the drug L-dopa which raises
dopamine levels they’d develop schizophrenic like symptoms.
It was found that antipsychotic drugs all blocked dopamine activity and the fact that
they alleviate symptoms like hallucinations and delusions shows us that dopamine
does have a role in schizophrenia.
Hyperdopaminergia in the Subcortex
This focuses on high levels of dopamine in the subcortex, for example, an excess of
dopamine receptors in Broca’s area (the area responsible for speech production)
could be associated with speech poverty and/or auditory hallucinations.
Hypodopaminergic in the Cortex
This focuses on abnormal dopamine systems in the brain’s cortex.Goldman-Rakic et
al.(2004) has found a role in how low levels of dopamine in the prefrontal cortex
(responsible for decision making and thinking) are responsible for the negative
symptoms of schizophrenia.
Neural Correlates of Schizophrenia
Neural correlated = Measurements of the structure or function of the brain that
correlates with an experience and may be implicated as the cause.
Neural Correlates of Negative Symptoms
Juckel et al. found abnormally lower activity in the ventral striatum (responsible for
the anticipation of a reward) in schizophrenics (this may be the cause of avolition
(loss of motivation) compared to controls and found a negative correlation between
its activity and the severity of overall negative symptoms of schizophrenia.
Neural Correlates of Positive Symptoms
