HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Seabrook, G. R Articles by Hutton, M. Search for Related Content PubMed PubMed Citation Articles by Seabrook, G. R Articles by Hutton, M.

BEYOND AMYLOID: The Next Generation of Alzheimer’s Disease Therapeutics

¹ Dept Alzheimer’s Research, Merck Research Laboratories, West Point, PA 19486
² Neuroscience Drug Discovery, Merck Research Laboratories, 33 Avenue Louis Pasteur, Boston, MA 02115

The precise pathological events that cause cognitive deficits in Alzheimer’s disease remain to be determined. The most widely held view is that accumulation of amyloid ß peptide initiates the disease process; however, with more than eighteen amyloid-based therapeutic candidates currently in clinical trials, the targeting of amyloid alone may not be sufficient to improve functional deficits over the course of the disease. Alternative targets, such as the tau protein and apolipoprotein E, have thus been increasingly investigated, and in the future, therapeutic strategies will likely address events that are upstream of a more broadly construed pathological cascade that includes but is not limited to the generation and accumulation of amyloid ß. Consideration of such events provides the basis for an "indirect amyloid hypothesis," for which data are beginning to emerge. Although it is clinically defined by simple post-mortem criteria, Alzheimer’s disease likely has a complex etiology, and effective treatments for this disease will become ever more urgent as the world’s population ages.