biological explanations for schizophrenia A01

• GENETICS

  -schizophrenia tends to run in families and the genetic explanation sees how schizophrenia is transmitted and is hereditary meaning it has been passed on by genes form an individuals family

  To prove genetics as a biological explanation for schizophrenia research often uses twin studies , family and adoption studies to assess concordance rates of developing schizophrenic and to assess the concordance rates of developing schizophrenia between different people of genetic readiness to assess the impact of genetics .
• Family studies

  -          In family studies the extend of the genetic relatedness is close and they usually compare parents to their offspring who they share 50% of their genetic make up with
• Family studies

  -          A family study carried out by Gottesman found that children with 2 schizophrenic parents had a concordance rate of 46% in comparison to children who had one schizophrenic apparent having a concordance rate of 13% and siblings had a concordance rate of 9% these finding suggests that there is a genetic ink as there was a higher concordance rate when there is a higher genetic similarity to the suffer of schizophrenia .
• Twin studies

  -          The extent of genetic relatedness is also high in twin studies since they compare the concordance rate in MZ twins who share 100% of their DNA to the concordance rate of DZ twins who share 50% of their DNA
• Twin studies

  -          Gottesman and Shield carried out a study 1996 where they used patient records from a psychiatric hospital over a period of 16 years and used 57 pairs of twins in their analysis – out of the 57 roughly half were MZ twins and they found the concordance rate in MZ twins was 54% and 18% for DZ twins – this suggest a genetic link as the MZ twins share exactly the same genes and have the higher concordance rate .
• Adoption studies

  -          Tienari et al in 2000 looked at 164 adoptees whose biological mother had been diagnosed with schizophrenia and out of those 6,75 of them also received a diagnosis of schizophrenia compared to 2% of the controlled adoptees who had non schizophrenic biological mothers . this then suggest a genetic link as there was a higher rate of schizophrenia in the biological similar relatives than when there was no genetic link
• *More recently gene mapping studies have been used to look for genetic material commonly found among sufferers . and this genetic research has found that there are a number of genes that appear to have an influence on the development of schizophrenia and so this is polygenic –
• *an example of one of these studies was carried out y Ripke et al in 2014 who combined data from the DNA of 36989 schizophrenics and 113000 non suffers to identify 128 independent genetic variation at 108 locations on human chromosomes that contribute most to developing schizophrenia – and they found that association were higher in genes expressed in the brain and genes associated with risk included those coding for the function of neurotransmitters including dopamine .
• NEURAL CORRELATES

  This explanation of schizophrenia seeks to find particular brain regions that are involved with schizophreniaboth positive and negative symptoms of schizophrenia have neural correlates
• NEURAL CORRELATES

  to investigate this research has used post mortems and FMRIs scans to measure brain activity whilst they complete tasks that schizophrenias struggle with
• NEURAL CORRELATESenlarged ventricles

  -          ventricles provide the supporting fluid for the brain and keep everything in place

  -          if there is damage to the brain and parts of it die the ventricles will enlarge to fill the space left

  -          Johnstone et al in 1976 found that schizophrenics had enlarged ventricles while non schizophrenics did not  which then indicates that schizophrenia is related to a loss of brain tissue
• Specific areas involved in schizophrenia.

  The prefrontal cortex

  -          Is the main area of the brain involved in executive control , reasoning and judgement and research has shown this part of the brain to be impaired ins schizophrenic patients , and it has been hypothesised that the cognitive symptoms of schizophrenia result from deficits within the prefrontal cortex and its connection with other areas of the brain , particularly the hippocampus

   
• Specific areas involved in schizophrenia.

  Broca’s area – in the frontal lobe

  -          is responsible for speech production.

  -          McGuire et al 1993 measured the cerebral blood flow in schizophrenic patients whilst they were experiencing hallucinations, and they found an increased blood flow in Broca’s area at the time which would suggest that this area of the brain is involved in producing auditory hallucinations.
• Specific areas involved in schizophrenia.

  The hippocampus

  -          Area of the brain in the temporal lobe

  -          Several studies have reported that anatomical changes in the hippocampus in schizophrenic patients – Conrad et al 1991.

  -          Deficits in the nerve connections between the hippocampus and the prefrontal cortex have been found to correlate with the degree of working memory impairments and a cognitive impairment in schizophrenia – Mukai et al 2015.
• Specific areas involved in schizophrenia.

  The hippocampus

  -          Goto and grace in 2008 suggested that hippocampal dysfunction might also influence levels of dopamine release in the basal ganglia which indirectly affects the processing of information in the prefrontal cortex.
• Specific areas involved in schizophrenia.

  Grey matter

  -          Schizophrenic individuals have a reduced volume of grey matter in their brain especially in the temporal and frontal lobes.

  -          Research ahs found many with schizophrenia particularly those displaying negative symptoms have enlarged ventricles – which are brain cavities filed with cerebrospinal fluid – found by Hartberg et al 2011.

   
• Specific areas involved in schizophrenia.

  Grey matter

  -          Enlarged ventricles are thought to be the consequence of nearby parts of the brain not developing properly or being damaged

  -          Cannon et al 2014 found that individuals at high clinical risk who develop schizophrenia showed a steeper rate of grey matter loss and a greater rate of expansion of the brain ventricles (enlarged ventricles) compared to those who did not develop schizophrenia.

   
• Specific areas involved in schizophrenia.

  White matter

  -          Found in the brain and spinal cord and is made up of nerve fibres covered in myelin which creates an insulating sheath around the nerve fibres and helps to conduct information quicky through the central nervous system enabling efficient information processing.

  -          Du et al 2013 found reduced myelination of white matter pathways in schizophrenic patients, compared to healthy patients – the controls – which was particularly found to be the case in the neural pathways between the prefrontal cortex and the hippocampus.
• Specific areas involved in schizophrenia.

  Wernicke’s area – temporal lobe

  -          Involved in understanding speech.

  -          Overactivity in this area of the brain can create auditory hallucinations which are illusions that are internally generated thoughts or voices are real coming from the outside.
• Specific areas involved in schizophrenia.

  Ventral Striatum

  -          This is a part of the limbic system and is involved in anticipating rewards.

  -          So, we can expect an area like this to be involved in the development of avolition.
• Specific areas involved in schizophrenia.

  Ventral Striatum

  -          Juckel et al in 2006 measured activity levels in the ventral striatum in schizophrenic individuals and found lower levels of activity in them than in the control observedthey also observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.

  -          Therefore, lower brain activity levels in this area are associated with more severe symptoms of schizophrenia.
• The dopamine hypothesis

  -          Schizophrenia is though to be caused by an imbalance of the neurotransmitter dopamine. which is why research into neural correlates of schizophrenia has focused on the important role of dopamine and on areas of the brain that are influential in the onset and development of schizophrenia
• The dopamine hypothesis

  -          neurotransmitters pass messages across the synapse and dopamine is involved in pleasure and reward motivation behaviour.
• The dopamine hypothesis

  -          Dopamine acts to increase the rate of firing of neurons during synaptic transmissionit was original believed that schizophrenia was a result of an over sensitivity to dopamine at the receptor sites however it is now knowledge that it is ore complex than this and that a deficit in dopamine itself is also linked to schizophrenia – and there is rather too much or too little dopamine
• dopamine hypothesis

   

  -          The revised dopamine hypothesis =Davis + Kahn 1991 proposed that positive symptoms are caused by too much dopamine in the subcortical areas of the brain particularly in the mesolimbic pathways and that the negative and cognitive symptoms are thought to rise from a deficit of dopamine in areas of the prefrontal cortexPatel et al 2010 using PET scans to assess dopamine levels ins schizophrenic and normal individuals – and found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared with their normal controls
• dopamine hypothesis  

  -          Drugs that decrease dopaminergic activity = are antipsychotics which all have one thing in common – they block the activity of dopamine in the brain
•  

  dopamine hypothese

  -          and by reducing activity in the neural pathways of the brain that use dopamine as the neurotransmitter – the drugs eliminate the positive symptoms of schizophrenia like hallucinations / delusions (antipsychotics decrease positive symptoms of schizophrenia)these drugs are known as dopamine antagonists because they block its action and alleviated many symptoms of schizophrenia which strengthens the case that dopamine plays an important role in the disorder
•  dopamine hypothesis

  -          Drugs that increase dopaminergic activity = amphetamine is a dopamine agonist , which stimulates nerves containing dopamine causing the synapse to be flooded with dopamine – so normal individuals exposed to this much dopamine caused by the drug can develop schizophrenic characteristics of a schizophrenic episode since they have too much dopamine but general disappears in the absence of the drug
•  dopamine hypothesis

  -          It may be that both hyperdopmainergia and hypodopmaninergia are both correct explanations for schizophrenia which explain how both high and low levels of dopamine in different regions of the brain are responsible for schizophrenia.

   

   
• Too much dopamine

  -          Dopamine hypothesis – claims that an excess of dopamine in certain areas of the brain are associated with positive symptoms of schizophrenia and suggest that schizophrenias commonly have abnormally high levels of D2 receptors on receiving neurons which results in more dopamine binding and therefore more neurons firing
• Too much dopamine

  -          Hyperdopaminergia in the subcortex – when there is too much dopaminein the original version of the dopamine hypothesis the focus was mainly on the role of high activity levels of dopamine in the subcortex
• Too much dopamine

  -          schizophrenics are thought to have an excess of dopamine (D2)receptors on receiving neurons which results in more dopamine binding and therefore more neurons firingand this occurs in the Broca’s area of the brain – responsible for speech production and this may then be associated with poverty of speech and or experiences of sudatory hallucinationssymptoms of hallucinations and such are positive symptoms of schizophrenia therefore too much dopamine causes positive symptoms of schizophrenia
• Too much dopamine

  -          in the Broca’s are if there is too much dopamine = positive symptoms
• Too little dopamine

  -          Hypodopaminergia in the cortex is when there is too little dopamine
• Too little dopamine

  -          more recent versions of the dopamine hypothesis have focussed instead on abnormal dopamine systems in the brains cortex which do not produce sufficient amounts of dopamine
• Too little dopamine

  -          Davis et al in 1991 highlighted that the prefrontal cortex does not have D2 receptors and instead it has D1 receptors so there is not just D2 receptors involvedand it may be this and the reduced dopamine in the frontal part of the brain which is causing the negative symptoms
• Too little dopamine

  -          Goldman – Rakic et al in 2004 then identified a role for low levels of dopamine in the prefrontal cortex which is responsible for decision making which is responsible for negative symptoms of schizophrenia
• Too little dopamine

  -          too little dopamine = negative symptoms

  in the prefrontal cortex if there is too little dopamine = negative symptoms