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From the Departments of Neurosciences (Drs. Masliah and Hansen, M. Mallory, M. Alford, and R. DeTeresa) and Pathology (Drs. Masliah and Hansen), School of Medicine, University of California, San Diego, La Jolla; and Departments of Neurology (Dr. Morris) and Pathology (Drs. McKeel and Morris), Washington University School of Medicine, St. Louis, MO.
Address correspondence and reprint requests to Dr. E. Masliah, Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093-0624; e-mail: emasliah @ucsd.edu
The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. Compared with control subjects (CDR = 0), mild (early) AD (CDR = 0.5 to 1) cases had a 25% loss of synaptophysin immunoreactivity. Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins. Thus, synaptic injury in frontal cortex is an early event in AD.
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