Requiring an amyloid-β1-42 biomarker for prodromal Alzheimer's disease or mild cognitive impairment does not lead to more efficient clinical trials

Alzheimer's and Dementia

Volumn 7, Issue 2, 2011, Pages 245-246

  Donohue, Michael C ^a   Gamst, Anthony C ^a   Aisen, Paul S ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN[1-42];

ALZHEIMER DISEASE; CEREBROSPINAL FLUID; CLINICAL TRIAL (TOPIC); LETTER; MILD COGNITIVE IMPAIRMENT; PRIORITY JOURNAL; SAMPLE SIZE; TREATMENT RESPONSE;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; BIOLOGICAL MARKERS; CLINICAL TRIALS AS TOPIC; COGNITION DISORDERS; HUMANS; PEPTIDE FRAGMENTS; RESEARCH DESIGN;

EID: 79952730827     PISSN: 15525260     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.jalz.2010.12.013     Document Type: Letter

References (2)

1. 1-42 biomarker for prodromal Alzheimer's disease or mild cognitive impairment does not lead to more efficient clinical trials. Alzheimers Dement 2010;6:367-77.
2. van Rossum IA, Vos S, Handels R. Visser. Biomarkers as predictors for conversion from mild cognitive impairment to Alzheimer-type dementia: implications for trial design. J Alzheimers Dis 2010;20:881-91.