Journal
PROGRESS IN NEUROBIOLOGY
Volume 93, Issue 1, Pages 13-U7Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2010.09.004
Keywords
Myelin; Gene expression; Genetic association; Brain imaging; Oligodendrocyte; Synaptic plasticity; Dopamine; Glutamate
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Funding
- Conte Center for the Neuroscience of Mental Disorders (NIMH) [P50MH066392]
- Mitsubishi Pharma Research Foundation
- Stanley Medical Foundation [06R-1427]
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH066392] Funding Source: NIH RePORTER
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Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem brains, and genetic association studies, have implicated oligodendrocyte and myelin dysfunction in this disease. Recent studies suggest that oligodendrocyte and myelin dysfunction leads to changes in synaptic formation and function, which could lead to cognitive dysfunction, a core symptom of schizophrenia. Furthermore, there is accumulating data linking oligodendrocyte and myelin dysfunction with dopamine and glutamate abnormalities, both of which are found in schizophrenia. These findings implicate oligodendrocyte and myelin dysfunction as a primary change in schizophrenia, not only as secondary consequences of the illness or treatment. Strategies targeting oligodendrocyte and myelin abnormalities could therefore provide therapeutic opportunities for patients suffering from schizophrenia. (C) 2010 Elsevier Ltd. All rights reserved.
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