The Ulas and Cotman article is of considerable interest in relation to a manuscript we will be publishing in the Archives of Neurology in October 1997 which sets forth a new hypothesis linking neurodegeneration in AD to a deficit in the NMDA receptor system. It has previously been shown by 4 or 5 laboratories that NMDA receptor binding and the functional status of the NMDA receptor are markedly decreased in both aging and AD. The Ulas and Cotman data take this one step further and show that in certain regions of the AD brain the deficit is more severe than in normal aging and the deficit is reflected specifically in a loss of expression of a specific NMDA receptor subunit (NMDAR1). A major problem with this line of research which the present study does not resolve is that it is not clear whether the changes in the NMDA receptor system are primary and of causal significance or are secondary to some other mechanism that is causing loss of neurons that express NMDAR1.
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The Ulas and Cotman article is of considerable interest in relation to a manuscript we will be publishing in the Archives of Neurology in October 1997 which sets forth a new hypothesis linking neurodegeneration in AD to a deficit in the NMDA receptor system. It has previously been shown by 4 or 5 laboratories that NMDA receptor binding and the functional status of the NMDA receptor are markedly decreased in both aging and AD. The Ulas and Cotman data take this one step further and show that in certain regions of the AD brain the deficit is more severe than in normal aging and the deficit is reflected specifically in a loss of expression of a specific NMDA receptor subunit (NMDAR1). A major problem with this line of research which the present study does not resolve is that it is not clear whether the changes in the NMDA receptor system are primary and of causal significance or are secondary to some other mechanism that is causing loss of neurons that express NMDAR1.
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