期刊
NEURON
卷 69, 期 2, 页码 203-213出版社
CELL PRESS
DOI: 10.1016/j.neuron.2011.01.002
关键词
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资金
- National Institutes of Health [AG05142]
- University of Southern California Alzheimer's Disease Research Center
- Myriad Genetics
- Lundbeck Inc.
- Elan Pharmaceuticals
- Sonexa Therapeutics
- Kareus Therapeutics
- Alzheimer's Association
- AstraZeneca Pharmaceuticals
- Baxter International Inc.
- Johnson Johnson Inc.
- Eli Lilly and Company
- Myriad Pharmaceuticals Inc.
- Novartis Pharmaceuticals Corporation
- Pfizer Incorporated
- Wyeth
- Takeda Pharmaceutical Company Ltd.
- Abbott Laboratories
- AC Immune
- GlaxoSmithKline
- Ipsen Group
- H. Lundbeck A/S
- Merck Co Inc.
- F. Hoffman-La Roche Ltd.
- Sanofi-aventis LLC
- Servier Laboratories
- Schwabe Pharmaceuticals
- Toyama Pharmaceutical Co. Ltd.
- Transition Therapeutics Inc.
- [AG020206]
Most current Alzheimer's disease (AD) therapies in advanced phases of development target amyloid beta-peptide (A beta) production, aggregation, or accumulation. Translational models suggest that anti-A beta 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-A beta 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 A beta 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.
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