Cerebral small vessel disease in middle age and genetic predisposition to late-onset Alzheimer's disease.

Autor:	Stefaniak JD; Manchester Academic Health Sciences Centre, Salford Royal NHS Foundation Trust, Salford, UK., Su L; Department of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK; China-UK Centre for Cognition and Ageing Research, Faculty of Psychology, Southwest University, Chongqing, China., Mak E; Department of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK., Sheikh-Bahaei N; Department of Radiology, University of Cambridge School of Clinical Medicine, Cambridge, UK., Wells K; The Centre for Mental Health, Imperial College, London, UK., Ritchie K; INSERM Unit 1061 Neuropsychiatry, Montpellier, France; University of Montpellier, Montpellier, France; Centre for Dementia Prevention, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK., Waldman A; Centre for Dementia Prevention, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK., Ritchie CW; Centre for Dementia Prevention, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK., O'Brien JT; Department of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK; Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK. Electronic address: john.obrien@medschl.cam.ac.uk.
Jazyk:	angličtina
Zdroj:	Alzheimer's & dementia : the journal of the Alzheimer's Association [Alzheimers Dement] 2018 Feb; Vol. 14 (2), pp. 253-258. Date of Electronic Publication: 2017 Nov 21.
DOI:	10.1016/j.jalz.2017.08.017
Abstrakt:	Introduction: 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. (Copyright © 2017 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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