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Memantine as a neuroprotective treatment in schizophrenia

Published online by Cambridge University Press:  02 January 2018

G. S. J. Rands*
Affiliation:
Camden and Islington Mental Health and Social Care Trust, and Department of Mental Health Sciences, Royal Free and UCL Medical School, Archway Campus, Highgate Hill, London N19 5NF, UK. E-mail: [email protected]
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Abstract

Type
Columns
Copyright
Copyright © 2005 The Royal College of Psychiatrists 

Phospholipid metabolism occurs in cell (including neuron) membranes and although regional differences are described by Jensen et al (Reference Jensen, Miller and Williamson2004), these are not neurotransmitter-specific. This research suggests increased phospholipid metabolism in the anterior cingulate area of people with schizophrenia.

Jensen et al suggest that this is supportive evidence for a neurodegenerative mechanism in schizophrenia. They also review the effects of neuroleptic and anxiolytic (including benzodiazepine) medications on brain phosphorus metabolism.

Memantine is a drug currently licensed for use in people with moderate to severe Alzheimer's dementia. It is a non-competitive, low-affinity N-methyl-d-aspartate (NMDA) antagonist. (The NMDA receptor is a class of glutamate receptor.) Glutamate-mediated excitotoxicity and/or receptor dysfunction is involved in the pathogenesis of several neuropsychiatric and neurological disorders. Memantine partially blocks these NMDA receptors, preventing a neurotoxic influx of calcium. Theoretically, it is neuroprotective for glutamate-receiving neurons.

Given its mode of action, it should theoretically be more effective in the early stages of neurodegenerative disorders such as Alzheimer's dementia. On these theoretical grounds it may also be neuroprotective for people with schizophrenia.

References

Jensen, J. E., Miller, J., Williamson, P. C., et al (2004) Focal changes in brain energy and phospholipid metabolism in first-episode schizophrenia: 31P-MRS chemical shift imaging study at 4 Tesla. British Journal of Psychiatry, 184, 409415.Google Scholar
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