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Neuron. 2011 Jan 27;69(2):203-13. doi: 10.1016/j.neuron.2011.01.002.

Anti-aβ therapeutics in Alzheimer's disease: the need for a paradigm shift.

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  • 1Center for Translational Research in Neurodegenerative Disease and Department of Neuroscience, College of Medicine, University of Florida, 1275 Center Drive BMS J-483, P.O. Box 100159, Gainesville, FL 32610-0244, USA. tgolde@mbi.ufl.edu

Abstract

Most current Alzheimer's disease (AD) therapies in advanced phases of development target amyloid β-peptide (Aβ) production, aggregation, or accumulation. Translational models suggest that anti-Aβ therapies may be highly effective if tested as agents to prevent or delay development of the disease or as therapies for asymptomatic patients with very early signs of AD pathology. However, anti-Aβ therapeutics are currently being tested in symptomatic patients where they are likely to be much less effective or ineffective. The lack of alignment between human clinical studies and preclinical studies, together with predictions about optimal trial design based on our understanding of the initiating role of Aβ aggregates in AD, has created a treatment versus prevention dilemma. In this perspective, we discuss why it is imperative to resolve this dilemma and suggest ways for moving forward in the hopes of enhancing the development of truly effective AD therapeutics.

© 2011 Elsevier Inc. All rights reserved.

PMID:
21262461
[PubMed - indexed for MEDLINE]
PMCID:
PMC3058906
Free PMC Article
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