TY - JOUR
T1 - Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease
AU - the Dominantly Inherited Alzheimer Network
AU - Brown, Belinda M.
AU - Sohrabi, Hamid R.
AU - Taddei, Kevin
AU - Gardener, Samantha L.
AU - Rainey-Smith, Stephanie R.
AU - Peiffer, Jeremiah J.
AU - Xiong, Chengjie
AU - Fagan, Anne M.
AU - Benzinger, Tammie
AU - Buckles, Virginia
AU - Erickson, Kirk I.
AU - Clarnette, Roger
AU - Shah, Tejal
AU - Masters, Colin L.
AU - Weiner, Michael
AU - Cairns, Nigel
AU - Rossor, Martin
AU - Graff-Radford, Neill R.
AU - Salloway, Stephen
AU - Vöglein, Jonathan
AU - Laske, Christoph
AU - Noble, James
AU - Schofield, Peter R.
AU - Bateman, Randall J.
AU - Morris, John C.
AU - Martins, Ralph N.
N1 - Funding Information:
Data collection and sharing for this project was supported by the Dominantly Inherited Alzheimer Network (DIAN; UF1 AG032438 ; to R.J.B. and J.C.M.) funded by the National Institute on Aging , the German Center for Neurodegenerative Diseases (DZNE), the Medical Research Council Dementias Platform UK (M.R.) ( MR/L023784/1 and MR/009076/1 ), and National Institute for Health Research Queen Square Dementia Biomedical Research Unit . B.M.B. received research support from the Alzheimer's Australia Dementia Research Foundation (G1001605), NHMRC National Institute of Dementia (APP1097105), and the Brain Foundation . J.C.M. and R.J.B. received research support from the National Institute of Health . This manuscript has been reviewed by DIAN study investigators for scientific content and consistency of data interpretation with previous DIAN study publications. The DIAN Expanded Registry welcomes contact from any families or treating clinicians interested in research about autosomal dominant familial Alzheimer's disease.
Funding Information:
R.J.B. reports grants from Eli Lilly, Roche, Pharma Consortium (AbbVie, AstraZeneca, Biogen, Eisai, Eli Lilly and Company, Hoffmann La-Roche Inc, Janssen, Pfizer, Sanofi-Aventis), and Tau SILK/PET Consortium (Biogen/AbbVie/Lilly); nonfinancial support from Avid Radiopharmaceuticals; personal fees and other from Washington University; personal fees and nonfinancial support from Roche, IMI, FORUM, and Pfizer; and personal fees from Merck, Johnson and Johnson, outside the submitted work. J.C.M. is currently participating in clinical trials of antidementia drugs from Eli Lilly and Company, Biogen, and Janssen. J.C.M. serves as a consultant for Lilly USA and receives research support from Eli Lilly/Avid Radiopharmaceuticals. T.B. receives grant funding from Avid Radiopharmaceuticals/Eli Lilly and participates in clinical trials sponsored by Eli Lilly, Avid Radiopharmaceuticals, Roche, and Pfizer. All other authors have declared no conflicts of interest.
Publisher Copyright:
© 2017 the Alzheimer's Association
PY - 2017/11
Y1 - 2017/11
N2 - Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42 and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.
AB - Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42 and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.
KW - Alzheimer's disease
KW - Amyloid β
KW - Dementia
KW - Genetics
KW - Physical activity
KW - Tau
UR - http://www.scopus.com/inward/record.url?scp=85019098030&partnerID=8YFLogxK
U2 - 10.1016/j.jalz.2017.03.008
DO - 10.1016/j.jalz.2017.03.008
M3 - Article
C2 - 28501451
AN - SCOPUS:85019098030
VL - 13
SP - 1197
EP - 1206
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
SN - 1552-5260
IS - 11
ER -