TY - JOUR
T1 - Variables associated with hippocampal atrophy rate in normal aging and mild cognitive impairment
AU - Alzheimer's Disease Neuroimaging Initiative
AU - Nosheny, Rachel L.
AU - Insel, Philip S.
AU - Truran, Diana
AU - Schuff, Norbert
AU - Jack, Clifford R.
AU - Aisen, Paul S.
AU - Shaw, Leslie M.
AU - Trojanowski, John Q.
AU - Weiner, Michael W.
N1 - Funding Information:
Data collection and sharing for this project was funded by the ADNI (National Institutes of Health Grant U01 AG024904 ). ADNI is funded by the National Institute on Aging , the National Institute of Biomedical Imaging and Bioengineering , and through generous contributions from Abbott , AstraZeneca AB , Bayer Schering Pharma AG , Bristol-Myers Squibb , Eisai Global Clinical Development , Elan , Genentech , GE Healthcare , GlaxoSmithKline , Innogenetics , Johnson and Johnson , Eli Lilly and Co , Medpace Inc , Merck & Co, Inc , Novartis AG , Pfizer Inc , F. Hoffman-La Roche , Schering-Plough , Synarc Inc , as well as nonprofit partners the Alzheimer's Association and Alzheimer Drug Discovery Foundation , with participation from the U.S. Food and Drug Administration . Private sector contributions to ADNI are facilitated by the Foundation for the National Institutes of Health ( www.fnih.org ). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Disease Cooperative Study at the University of California, San Diego. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of California, Los Angeles.
Funding Information:
To fully address any financial relationships of the coauthors that may lead to a perceived conflict of interest, we would like to make the following disclosures. Dr Shaw reports grants from NIA/NIH during the conduct of the study. Dr Shaw previously was consultant for Innogenetics and collaborates on quality assessment activities as part of the Alzheimer's Disease Neuroimaging Initiative. Dr Aisen has been a consultant for NeuroPhage; Elan Corporation, Wyeth, Eisai Inc, Schering-Plough Corp, Bristol-Myers Squibb, Eli Lilly and Company, NeuroPhage, Merck & Co, Roche, Amgen, Genentech, Inc, Abbott, Pfizer Inc, Novartis, Bayer, Astellas, Dainippon, Biomarin, Solvay, Otsuka, Daiichi, AstraZeneca, Janssen, Medivation, Inc, Ichor, Toyama, Lundbeck, Biogen Idec, iPerian, Probiodrug, Somaxon, Biotie, Anavex, and Kyowa Hakko Kirin Pharma. In addition, Dr Aisen has grants or pending grants from Lilly, Baxter, NIA, and FNIH. Dr Weiner has been on scientific advisory boards for Pfizer and BOLT Inter-national; has been a consultant for Pfizer Inc, Janssen, KLJ Associates, Easton Associates, Harvard University, inThought, INC Research, Inc, University of California, Los Angeles, Alzheimer's Drug Discovery Foundation and Sanofi-Aventis Groupe; has received funding for travel from Pfizer, AD PD meeting, Paul Sabatier University, Novartis, Tohoku University, MCI Group, France, Travel eDreams, Inc, Neuroscience School of Advanced Studies (NSAS), Danone Trading, BV, CTAD ANT Congres; serves as an associate editor of Alzheimer's & Dementia; has received honoraria from Pfizer, Tohoku University, and Danone Trading, BV; has research support from Merck, Avid, DOD, and VA; and has stock options in Synarc and Elan.
Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/1/1
Y1 - 2015/1/1
N2 - The goal of this study was to identify factors contributing to hippocampal atrophy rate (HAR) in clinically normal older adults (NC) and participants with mild cognitive impairment (MCI). Longitudinal HAR was measured on T1-weighted magnetic resonance imaging, and the contribution of age, gender, apolipoprotein E (ApoE) ε4 status, intracranial volume, white matter lesions, and β-amyloid (Aβ) levels to HAR was determined using linear regression. Age-related effects of HAR were compared in Aβ positive (Aβ+) and Aβ negative (Aβ-) participants. Age and Aβ levels had independent effects on HAR in NC, whereas gender, ApoE ε4 status, and Aβ levels were associated with HAR in MCI. In multivariable models, Aβ levels were associated with HAR in NC; ApoE ε4 and Aβ levels were associated with HAR in MCI. In MCI, age was a stronger predictor of HAR in Aβ- versus Aβ+ participants. HAR was higher in Aβ+ participants, but most of the HAR was because of factors other than Aβ status. Age-related effects on HAR did not differ between NC versus MCI participants with the same Aβ status. Therefore, we conclude that even when accounting for other covariates, Aβ status, and not age, is a significant predictor of HAR; and that most of the HAR is not accounted for by Aβ status in either NC or MCI.
AB - The goal of this study was to identify factors contributing to hippocampal atrophy rate (HAR) in clinically normal older adults (NC) and participants with mild cognitive impairment (MCI). Longitudinal HAR was measured on T1-weighted magnetic resonance imaging, and the contribution of age, gender, apolipoprotein E (ApoE) ε4 status, intracranial volume, white matter lesions, and β-amyloid (Aβ) levels to HAR was determined using linear regression. Age-related effects of HAR were compared in Aβ positive (Aβ+) and Aβ negative (Aβ-) participants. Age and Aβ levels had independent effects on HAR in NC, whereas gender, ApoE ε4 status, and Aβ levels were associated with HAR in MCI. In multivariable models, Aβ levels were associated with HAR in NC; ApoE ε4 and Aβ levels were associated with HAR in MCI. In MCI, age was a stronger predictor of HAR in Aβ- versus Aβ+ participants. HAR was higher in Aβ+ participants, but most of the HAR was because of factors other than Aβ status. Age-related effects on HAR did not differ between NC versus MCI participants with the same Aβ status. Therefore, we conclude that even when accounting for other covariates, Aβ status, and not age, is a significant predictor of HAR; and that most of the HAR is not accounted for by Aβ status in either NC or MCI.
KW - Alzheimer's disease
KW - Hippocampal atrophy rate
KW - Longitudinal study
KW - Normal aging
KW - β-amyloid
UR - http://www.scopus.com/inward/record.url?scp=84920495244&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84920495244&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2014.07.036
DO - 10.1016/j.neurobiolaging.2014.07.036
M3 - Article
C2 - 25175807
AN - SCOPUS:84920495244
VL - 36
SP - 273
EP - 282
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
IS - 1
ER -