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Cerebral small vessel disease in middle age and genetic predisposition to late‐onset Alzheimer's disease
Author(s) -
Stefaniak James D.,
Su Li,
Mak Elijah,
SheikhBahaei Nasim,
Wells Katie,
Ritchie Karen,
Waldman Adam,
Ritchie Craig W.,
O'Brien John T.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.08.017
Subject(s) - hyperintensity , dementia , genetic predisposition , apolipoprotein e , disease , medicine , family history , white matter , age of onset , pathology , cardiology , magnetic resonance imaging , radiology
Cerebral small vessel disease (CSVD) is associated with late‐onset Alzheimer's disease (LOAD) and might contribute to the relationship between apolipoprotein E ε4 ( APOE ε4) and LOAD, in older people. However, it is unclear whether CSVD begins in middle age in individuals genetically predisposed to LOAD. Methods We assessed the relationship between radiological markers of CSVD, white matter hyperintensities and microbleeds, and genetic predisposition to LOAD in a cross‐sectional analysis of cognitively normal subjects aged 40–59 years recruited from the PREVENT Dementia study. Results Microbleed prevalence was 14.5%, and mean ± standard deviation white matter hyperintensity percentage of total brain volume was 0.41 ± 0.28%. There was no significant association between APOE ε4 carrier status or history of parental dementia and white matter hyperintensity volume ( P = .713, .912 respectively) or microbleeds ( P = .082, .562 respectively) on multiple regression. Discussion Genetic predisposition to LOAD, through APOE genotype or AD family history, is not associated with CSVD in middle age.