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Requiring an amyloid‐β 1–42 biomarker for prodromal Alzheimer's disease or mild cognitive impairment does not lead to more efficient clinical trials
Author(s) -
Donohue Michael C.,
Gamst Anthony C.,
Aisen Paul S.
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.12.013
Subject(s) - citation , cognitive impairment , library science , gerontology , psychology , medicine , disease , computer science
To the Editor, Dr. Schneider and coauthors [1] have performed an interesting simulation study and present provocative results suggesting that there is no advantage to conducting clinical trials on predementia populations defined by low levels of amyloid peptide in cerebrospinal fluid. These results appear to be at odds with other analyses [2]. The differences can be explained, in part, by the assumptions regarding treatment