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Brief Communications
January 9, 2001

Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease

January 9, 2001 issue
56 (1) 127-129

Abstract

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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Information & Authors

Information

Published In

Neurology®
Volume 56Number 1January 9, 2001
Pages: 127-129
PubMed: 11148253

Publication History

Received: April 26, 2000
Accepted: August 24, 2000
Published online: January 9, 2001
Published in print: January 9, 2001

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Authors

Affiliations & Disclosures

E. Masliah, MD
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.
M. Mallory, BS
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.
M. Alford, BS
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.
R. DeTeresa, BS
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.
L.A. Hansen, MD
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.
D.W. McKeel, Jr., MD
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.
J.C. Morris, MD
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.

Notes

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

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