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dc.contributor.authorJavitt, Daniel C.
dc.contributor.authorSchoepp, Darryle
dc.contributor.authorKalivas, Peter W.
dc.contributor.authorVolkow, Nora D.
dc.contributor.authorZarate, Carlos
dc.contributor.authorMerchant, Kalpana
dc.contributor.authorBear, Mark
dc.contributor.authorUmbricht, Daniel
dc.contributor.authorHajos, Mihaly
dc.contributor.authorPotter, William Z.
dc.contributor.authorLee, Chi-Ming
dc.date.accessioned2012-02-22T21:23:44Z
dc.date.available2012-02-22T21:23:44Z
dc.date.issued2011-09
dc.date.submitted2011-06
dc.identifier.issn1946-6242
dc.identifier.issn1946-6234
dc.identifier.urihttp://hdl.handle.net/1721.1/69162
dc.description.abstractThe neurotransmitter glutamate is the primary excitatory neurotransmitter in mammalian brain and is responsible for most corticocortical and corticofugal neurotransmission. Disturbances in glutamatergic function have been implicated in the pathophysiology of several neuropsychiatric disorders—including schizophrenia, drug abuse and addiction, autism, and depression—that were until recently poorly understood. Nevertheless, improvements in basic information regarding these disorders have yet to translate into Food and Drug Administration–approved treatments. Barriers to translation include the need not only for improved compounds but also for improved biomarkers sensitive to both structural and functional target engagement and for improved translational models. Overcoming these barriers will require unique collaborative arrangements between pharma, government, and academia. Here, we review a recent Institute of Medicine–sponsored meeting, highlighting advances in glutamatergic theories of neuropsychiatric illness as well as remaining barriers to treatment development.en_US
dc.description.sponsorshipNational Institute of Mental Health (U.S.) (grant R37MH49334)en_US
dc.description.sponsorshipNational Institute of Mental Health (U.S.) (Intramural Research Program)en_US
dc.description.sponsorshipNational Institute of Mental Health (U.S.) (R01DA03383)en_US
dc.description.sponsorshipNational Institute of Mental Health (U.S.) (P50MH086385)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.)en_US
dc.description.sponsorshipFRAXA Research Foundationen_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.description.sponsorshipSimons Foundationen_US
dc.language.isoen_US
dc.publisherAmerican Association for the Advancement of Scienceen_US
dc.relation.isversionofhttp://dx.doi.org/10.1126/scitranslmed.3002804en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourcePubMed Centralen_US
dc.titleTranslating Glutamate: From Pathophysiology to Treatmenten_US
dc.typeArticleen_US
dc.identifier.citationJavitt, David C. et al. “Translating Glutamate: From Pathophysiology to Treatment.” Science Translational Medicine 3.102 (2011): 102mr2–102mr2.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.approverBear, Mark
dc.contributor.mitauthorBear, Mark
dc.relation.journalScience Translational Medicineen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsJavitt, D. C.; Schoepp, D.; Kalivas, P. W.; Volkow, N. D.; Zarate, C.; Merchant, K.; Bear, M. F.; Umbricht, D.; Hajos, M.; Potter, W. Z.; Lee, C.-M.en
mit.licenseOPEN_ACCESS_POLICYen_US
mit.metadata.statusComplete


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