Translating Glutamate: From Pathophysiology to Treatment
Name
Bear-Translating Glutamate.pdf
Size
3.62 MB
Format
Adobe PDF
Checksum (MD5)
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Author(s)
Javitt, Daniel C.
Schoepp, Darryle
Kalivas, Peter W.
Volkow, Nora D.
Zarate, Carlos
Merchant, Kalpana
Bear, Mark
Umbricht, Daniel
Hajos, Mihaly
Potter, William Z.
Date Issued
September 2011
Journal
Science Translational Medicine
Publisher
American Association for the Advancement of Science
Citation
Javitt, David C. et al. “Translating Glutamate: From Pathophysiology to Treatment.” Science Translational Medicine 3.102 (2011): 102mr2–102mr2.
Version
Author's final manuscript
Abstract
The 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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike 3.0
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DOI of Published Version
https://doi.org/10.1126/scitranslmed.3002804
