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Glutamate and psychosis risk
Alice Egerton1, Paolo Fusar-Poli, James M Stone
1Department of Psychosis Studies, Institute of Psychiatry, King's Health Partners, King's College London, De Crespigny Park, Denmark Hill, London, UK. Alice.Egerton@kcl.ac.uk
Current Pharmaceutical Design
|January 14, 2012
Summary
Abnormalities in glutamatergic transmission are linked to psychosis risk. Early detection of these glutamatergic abnormalities suggests potential for psychosis prevention therapies.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Glutamatergic transmission abnormalities are increasingly implicated in psychosis risk.
- Genetic and environmental factors influencing psychosis risk converge on NMDA receptor signaling.
Purpose of the Study:
- To review evidence linking genetic and environmental risk factors to glutamatergic transmission in psychosis.
- To explore the potential of glutamatergic therapies for psychosis prevention.
Main Methods:
- Review of genetic polymorphisms, animal models, human neuroimaging, and in vivo magnetic resonance spectroscopy (MRS) studies.
- Analysis of how environmental risk factors (stress, cannabis, maternal infection) impact glutamatergic function.
Main Results:
- Genetic risk alleles for schizophrenia affect NMDA receptor signaling.
- Environmental risk factors induce glutamatergic dysfunction.
- MRS studies detect glutamatergic abnormalities in individuals at risk for psychosis.
Conclusions:
- Glutamatergic dysfunction may precede and contribute to psychosis onset, potentially via dopaminergic pathways.
- Early identification of glutamatergic abnormalities supports the development of novel therapeutic strategies for psychosis prevention.
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