TY - JOUR
T1 - Pittsburgh compound B imaging and prediction of progression from cognitive normality to symptomatic Alzheimer disease
AU - Morris, John C.
AU - Roe, Catherine M.
AU - Grant, Elizabeth A.
AU - Head, Denise
AU - Storandt, Martha
AU - Goate, Alison M.
AU - Fagan, Anne M.
AU - Holtzman, David M.
AU - Mintun, Mark A.
N1 - Funding Information:
This work has been supported by the National High Technology Research and Development Program of China (863 Program) (No.2013AA014200), the National Natural Science Foundation of China (No.11444001), and the Municipal Natural Science Foundation of Tianjin (No.14JCYBJC16500).
PY - 2009/12
Y1 - 2009/12
N2 - Objective: To determine whether preclinical Alzheimer disease (AD), as detected by the amyloid-imaging agent Pittsburgh Compound B (PiB) in cognitively normal older adults, is associated with risk of symptomatic AD. Design: A longitudinal cohort study of cognitively normal older adults assessed with positron emission tomography (PET) to determine the mean cortical binding potential for PiB and followed up with annual clinical and cognitive assessments for progression to very mild dementia of the Alzheimer type (DAT). Setting: The Alzheimer's Disease Research Center, Washington University, St Louis, Missouri. Participants: One hundred fifty-nine participants with a mean age of 71.5 years with a Clinical Dementia Rating (CDR) of 0 on a PET PiB scan at baseline. Main Outcome Measure: Progression from CDR 0 to CDR 0.5 status (very mild dementia). Results: Twenty-three participants progressed to CDR 0.5 at follow-up assessment (range, 1-5 assessments after PET PiB). Of these, 9 also were diagnosed with DAT. Higher mean cortical binding potential values for PiB (hazard ratio, 4.85; 95% confidence interval, 1.22-19.01; P=.02) and age (hazard ratio, 1.14; 95% confidence interval, 1.02-1.28; P=.03) predicted progression to CDR 0.5 DAT. The CDR 0.5 DAT group showed decline in 3 cognitive domains (episodic memory, semantic memory, and visuospatial performance) and had volume loss in the parahippocampal gyrus (includes entorhinal cortex) compared with individuals who remained at CDR 0. Conclusion: Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD.
AB - Objective: To determine whether preclinical Alzheimer disease (AD), as detected by the amyloid-imaging agent Pittsburgh Compound B (PiB) in cognitively normal older adults, is associated with risk of symptomatic AD. Design: A longitudinal cohort study of cognitively normal older adults assessed with positron emission tomography (PET) to determine the mean cortical binding potential for PiB and followed up with annual clinical and cognitive assessments for progression to very mild dementia of the Alzheimer type (DAT). Setting: The Alzheimer's Disease Research Center, Washington University, St Louis, Missouri. Participants: One hundred fifty-nine participants with a mean age of 71.5 years with a Clinical Dementia Rating (CDR) of 0 on a PET PiB scan at baseline. Main Outcome Measure: Progression from CDR 0 to CDR 0.5 status (very mild dementia). Results: Twenty-three participants progressed to CDR 0.5 at follow-up assessment (range, 1-5 assessments after PET PiB). Of these, 9 also were diagnosed with DAT. Higher mean cortical binding potential values for PiB (hazard ratio, 4.85; 95% confidence interval, 1.22-19.01; P=.02) and age (hazard ratio, 1.14; 95% confidence interval, 1.02-1.28; P=.03) predicted progression to CDR 0.5 DAT. The CDR 0.5 DAT group showed decline in 3 cognitive domains (episodic memory, semantic memory, and visuospatial performance) and had volume loss in the parahippocampal gyrus (includes entorhinal cortex) compared with individuals who remained at CDR 0. Conclusion: Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD.
UR - http://www.scopus.com/inward/record.url?scp=73549092137&partnerID=8YFLogxK
U2 - 10.1001/archneurol.2009.269
DO - 10.1001/archneurol.2009.269
M3 - Article
C2 - 20008650
AN - SCOPUS:73549092137
SN - 0003-9942
VL - 66
SP - 1469
EP - 1475
JO - Archives of neurology
JF - Archives of neurology
IS - 12
ER -