TY - JOUR
T1 - Association of education with Aβ burden in preclinical familial and sporadic Alzheimer disease
AU - DIAN Study Group and the PREVENT-AD Research Group
AU - Gonneaud, Julie
AU - Bedetti, Christophe
AU - Pichet Binette, Alexa
AU - Benzinger, Tammie L.S.
AU - Morris, John C.
AU - Bateman, Randall J.
AU - Poirier, Judes
AU - Breitner, John C.S.
AU - Villeneuve, Sylvia
N1 - Funding Information:
This work was supported by 2 Canada Research Chairs (S.V., J.C.S.B.), a Canadian Institutes of Health Research project grant PJT-148963 (S.V.), a Canada Fund for Innovation (S.V.), an Alzheimer's Association Research Grant NIRG-397028 (S.V.), the Lemaire foundation (J.P., S.V.), the J.L. Levesque Foundation (J.P.), a joint Alzheimer Society of Canada and Brain Canada Research grant NIG-17-08 (S.V.), a StoP-AD fellowship (J.G.), a Quebec Bio-Imaging Network scholarship (J.G.), and a joint FRQ-S and Alzheimer Society of Canada scholarship (A.P.B.). PREVENT-AD was funded by a $13.5 million, 7-year public–private partnership using funds provided by McGill University, the Fonds de Recherche du Québec–Santé (FRQ-S), an unrestricted research grant from Pfizer Canada, the Levesque Foundation, the Douglas Hospital Research Centre and Foundation, the Government of Canada, the Canada Fund for Innovation, and Genome Quebec Innovation Center (J.C.S.B., J.P.). Data collection and sharing for this project was also supported by The Dominantly Inherited Alzheimer's Network (DIAN, U19AG032438) funded by the National Institute on Aging (NIA), the German Center for Neurodegenerative Diseases (DZNE), Raul Carrea Institute for Neurological Research (FLENI), partial support by the Research and Development Grants for Dementia from Japan Agency for Medical Research and Development, AMED, and the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI).
Publisher Copyright:
© American Academy of Neurology.
PY - 2020/9/15
Y1 - 2020/9/15
N2 - Objective: To determine whether years of education and the ϵ4 risk allele at APOE influence β-amyloid (Aβ) pathology similarly in asymptomatic individuals with a family history of sporadic Alzheimer disease (AD) and presymptomatic autosomal dominant AD mutation carriers. Methods:We analyzed cross-sectional data from 106 asymptomatic individuals with a parental history of sporadic AD (PREVENT-AD cohort; age 67.28 ± 4.72 years) and 117 presymptomatic autosomal dominant AD mutation carriers (DIAN cohort; age 35.04 ± 9.43 years). All participants underwent structural MRI and Aβ-PET imaging. In each cohort we investigated the influence of years of education, APOE ϵ4 status, and their interaction on Aβ-PET. Results:Asymptomatic individuals with a parental history of sporadic AD showed increased Aβ burden associated with APOE ϵ4 carriage and lower level of education, but no interaction between these. Presymptomatic mutation carriers of autosomal dominant AD showed no relation between APOE ϵ4 and Aβ burden, but increasing level of education was associated with reduced Aβ burden. The association between educational attainment and Aβ burden was similar in the 2 cohorts. Conclusions:While the APOE ϵ4 allele confers increased tendency toward Aβ accumulation in sporadic AD only, protective environmental factors, like increased education, may promote brain resistance against Aβ pathology in both sporadic and autosomal dominant AD.
AB - Objective: To determine whether years of education and the ϵ4 risk allele at APOE influence β-amyloid (Aβ) pathology similarly in asymptomatic individuals with a family history of sporadic Alzheimer disease (AD) and presymptomatic autosomal dominant AD mutation carriers. Methods:We analyzed cross-sectional data from 106 asymptomatic individuals with a parental history of sporadic AD (PREVENT-AD cohort; age 67.28 ± 4.72 years) and 117 presymptomatic autosomal dominant AD mutation carriers (DIAN cohort; age 35.04 ± 9.43 years). All participants underwent structural MRI and Aβ-PET imaging. In each cohort we investigated the influence of years of education, APOE ϵ4 status, and their interaction on Aβ-PET. Results:Asymptomatic individuals with a parental history of sporadic AD showed increased Aβ burden associated with APOE ϵ4 carriage and lower level of education, but no interaction between these. Presymptomatic mutation carriers of autosomal dominant AD showed no relation between APOE ϵ4 and Aβ burden, but increasing level of education was associated with reduced Aβ burden. The association between educational attainment and Aβ burden was similar in the 2 cohorts. Conclusions:While the APOE ϵ4 allele confers increased tendency toward Aβ accumulation in sporadic AD only, protective environmental factors, like increased education, may promote brain resistance against Aβ pathology in both sporadic and autosomal dominant AD.
UR - http://www.scopus.com/inward/record.url?scp=85091127137&partnerID=8YFLogxK
U2 - 10.1212/WNL.0000000000010314
DO - 10.1212/WNL.0000000000010314
M3 - Article
C2 - 32759192
AN - SCOPUS:85091127137
SN - 0028-3878
VL - 95
SP - E1554-E1564
JO - Neurology
JF - Neurology
IS - 11
ER -