CARLSSON ET AL 99

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NETWORK INTERACTIONS IN SZ – THERAPEUTIC IMPLICATIONS. Awarded the Nobel Peace prize for their work on neural transmission.. Arvid. is best known for his work into the relationship between dopamine and Parkinson’s disease.. ID: 576805 Download Presentation

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CARLSSON ET AL 99




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Slide1

CARLSSON ET AL 99

NETWORK INTERACTIONS IN SZ – THERAPEUTIC IMPLICATIONS

Awarded the Nobel Peace prize for their work on neural transmission.

Arvid is best known for his work into the relationship between dopamine and Parkinson’s disease.

Slide2

METHODOLOGY

This is NOT a studyIt is a PAPER REVIEW of research findings

Published in a journalDoes not gather direct data

Obtained evidence about the role of neurotransmitters in SZ;Carlsson’s own workWork of othersAnimal research (rodents and primates)PET scansParkinson’s and Huntington’s patients

Slide3

GLUTAMATE

Most common neurotransmitter accounting for 90% of synaptic connectionsInvolved in learning and memoryRegulates development and creation of nerve contactsGlutamate bond to NMDA receptors

DOPAMINE

Controls the brains reward and pleasure centresFeelings of pleasure, addiction, movement and motivationPeople repeat behaviours that lead to dopamine production

Slide4

Professor Jeffrey Lieberman discusses the glutamate hypothesis of schizophrenia. The drug PCP acts on glutamate receptors, producing schizophrenia-like symptoms.

https://www.dnalc.org/view/1182-Glutamate-Hypothesis-of-Schizophrenia.html

Professor Daniel Weinberger discusses evidence from a number of research areas that highlight the importance of the neurotransmitter glutamate in schizophrenia

https://www.dnalc.org/view/1173-Glutamate-and-Schizophrenia.html

Watch

videos

Slide5

AIM

HYPERDOPAMINERGIA – high levels of dopamineHYPOGLUTAMTERGIA – low levels of glutamate

Dopamine hypothesis has been strengthened with improvement in technology showing more complex neural interactions with dopamine and other neurotransmitters (glutamate). Most patients complain about the side effects and quality of life when on antipsychotics.This has implications on the drugs given to SZ patients as a treatment need to be tested for effectiveness.Drugs that affect glutamate functioning may help to control negative symptoms of SZ

To produce drugs that REDUCE levels of relapse and negative side effects

Low levels of glutamate is associated with high dopamine levels

Slide6

RATIONALE

There is no ‘one cause’ for SZ

It follows that if neurotransmitter functioning cause SZ symptoms then drug treatments can help

Antipsychotic drugs work to suppress hallucinations and delusions

After 60 years of research, there are now likely safer antipsychotic medications, but they have failed to become more effective

overall

As more knowledge is uncovered about how neurotransmitters work together, the more we can improve and develop drug treatments

where

dopamine agonists

can mimic positive symptoms with significant risks to brain structures during and after use,

glutamate

antagonists

mimic some positive and negative symptoms with less brain harm

Slide7

AGREED FINDINGS

PCP

acts as an antagonist of a glutamate receptor

Glutamate deficiency more likely to be result in psychosis (

Moghaddam

& Adams 98)

Glutamate failure

in the cerebral cortex may lead to negative symptoms

In the basal ganglia may lead to positive symptoms

Clozapine is a highly effective drug for SZ

fewer reported side effects

Reduces levels of dopamine and serotonin

More effective in patients who have not previously responded to treatment

Slide8

ANIMAL STUDIES

Research done on mice in early 2009 has shown that administering NMDA antagonists in late/post foetal stage increases neuronal death which is linked to adult schizophrenia like behaviour. This led to symptoms (such as disturbed social function, inability to adapt to predictable future stressors) that overlap with schizophrenia.

Slide9

CONCLUSIONS

Further research is needed in developing drugs to treat SZ to avoid negative side effectsConsider the role of other neurotransmittersDifferent types of SZ could be due to abnormal levels of different neurotransmitters (not just DA)

Slide10

Conclusions….

How useful are drugs relating to dopamine?

Carlsson

et al. Explain that drugs have been developed that can stabilise The dopaminergic system without lowering levels of dopamine too far.

Why is this a concern?

Extrapyramidal side effects

There may be sub populations of those with SZ and there may be different causes of SZ within these sub populations.

Implications in terms of treatment? Individual differences?

Slide11

NMDA receptors regulate dopamine neuronsGlutamate bond to NMDA receptorsPCP is an NMDA antagonist reducing glutamate productionDopamine production is increased

Explain how NMDA receptor antagonists relate to glutamate deficiency [2]

Give evidence to show that limited glutamate might link to psychotic like symptoms [4]

Evidence from animal studies and neuroimaging is strong (

Carlsson

et al 99)

PCP acts

as an antagonist of a glutamate

receptor. Glutamate

deficiency more likely to be result in psychosis (

Moghaddam

& Adams 98)

Glutamate failure

in

the cerebral cortex may lead to negative

symptoms whereas

in

the basal ganglia may lead to positive symptoms

Research done on mice in early 2009 has shown that administering NMDA antagonists in late/post foetal stage increases neuronal death which is linked to adult schizophrenia like behaviour.

Slide12

EVALUTION

Research methodStrengthsLimitationsSECONDARY DATAPET SCANSANIMAL RESEARCH

Read the text

and

find evaluation points that link directly as method to study schizophrenia

Slide13

POINT

EXPLANTION/EXAMPLE

EXTENSION + comment


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