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Review
. 2009 Feb 19:7:7.
doi: 10.1186/1741-7015-7-7.

Recent developments in Alzheimer's disease therapeutics

Affiliations
Review

Recent developments in Alzheimer's disease therapeutics

Michael S Rafii et al. BMC Med. .

Abstract

Alzheimer's disease is a devastating neurological disorder that affects more than 37 million people worldwide. The economic burden of Alzheimer's disease is massive; in the United States alone, the estimated direct and indirect annual cost of patient care is at least $100 billion. Current FDA-approved drugs for Alzheimer's disease do not prevent or reverse the disease, and provide only modest symptomatic benefits. Driven by the clear unmet medical need and a growing understanding of the molecular pathophysiology of Alzheimer's disease, the number of agents in development has increased dramatically in recent years. Truly *'disease-modifying' therapies that target the underlying mechanisms of Alzheimer's disease have now reached late stages of human clinical trials. Primary targets include beta-amyloid, whose presence and accumulation in the brain is thought to contribute to the development of Alzheimer's disease, and tau protein which, when hyperphosphorylated, results in the self-assembly of tangles of paired helical filaments also believed to be involved in the pathogenesis of Alzheimer's disease. In this review, we briefly discuss the current status of Alzheimer's disease therapies under study, as well the scientific context in which they have been developed.

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References

    1. Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science. 2002;297:353–356. doi: 10.1126/science.1072994. - DOI - PubMed
    1. Gervais F. GAG mimetics: potential to modify underlying disease process in AD. Neurobiol Aging. 2004;25:S11–12.
    1. Aisen PS, Saumier D, Briand R, Laurin J, Gervais F, Tremblay P, Garceau D. A Phase II study targeting amyloid-beta with 3APS in mild-to-moderate Alzheimer disease. Neurology. 2006;67:1757–1763. doi: 10.1212/01.wnl.0000244346.08950.64. - DOI - PubMed
    1. Relkin NR. Current state of immunotherapy for Alzheimer's disease. CNS Spectr. 2008;13:39–41. - PubMed
    1. DeMattos RB, Bales KR, Cummins DJ, Paul SM, Holtzman DM. Brain to plasma amyloid-beta efflux: a measure of brain amyloid burden in a mouse model of Alzheimer's disease. Science. 2002;295:2264–2267. doi: 10.1126/science.1067568. - DOI - PubMed

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