A therapeutic target for Alzheimer's disease
Amyloid plaques, the characteristic lesions found in the brains of patients with Alzheimer's disease, are extracellular deposits of the beta-amyloid petide (Abeta). The production of Abeta peptide involves two enzymes: alpha-secretase and beta-secretase. Two studies in this issue (Nature Neuroscience, Vol. 4, No. 3, 01 Mar 2001) show that transgenic mice lacking the BACE1 isoform of the beta-secretase no longer produce the Abeta peptide. Vassar and colleagues could not measure any appreciable levels of Abeta peptide in the brains of these mutant mice, even when they were crossed with mice that overproduce the APP protein (the source of the Abeta peptide). In another paper, Wong and colleagues showed specifically that neurons from BACE1-deficient mutant mice failed to secrete Abeta peptide. The lack of secretion in BACE1 knockout mice was maintained even when the authors introduced the Swedish variant of APP, a mutation known to be associated with Alzheimer's disease. A big surprise from these studies is that deletion of the BACE1 secretase had no detrimental effects that could be detected on the viability or morphology of these mice. This identifies the BACE1 enzyme as a very appealing target for therapeutic intervention in Alzheimer's patients; drugs that inhibit BACE1 would block the production of Abeta peptide and would be predicted to have few side effects.
Dr. Philip C. Wong
Department of Pathology
Program in Cellular and Molecular Medicine
Johns Hopkins University School of Medicine
558 Ross Research Building, 720 Rutland Avenue
Baltimore, Maryland 21205-2196
tel: +1 410-502-5168
fax: +1 410-955-9777
Dr. Robert Vassar
One Amgen Center Drive
Thousand Oaks, California 91320
tel: +1 805-447-1289
fax: +1 805-480-1347
(C) Nature Neuroscience press release.
Message posted by: Trevor M. D'Souza
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