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From the Department of Neurology (Drs. Federoff and Kurlan) and Center for Aging and Developmental Biology (Drs. Coleman, Federoff, and Kurlan), University of Rochester School of Medicine, NY.
Address correspondence and reprint requests to Dr. R. Kurlan, University of Rochester School of Medicine, 601 Elmwood Ave., Rochester, NY 14642-8673; e-mail: Roger_Kurlan{at}urmc.rochester.edu
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.
Received August 14, 2003. Accepted in final form April 12, 2004.
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