Cognitive reserve and midlife vascular risk: Cognitive and clinical outcomes.


Journal

Annals of clinical and translational neurology
ISSN: 2328-9503
Titre abrégé: Ann Clin Transl Neurol
Pays: United States
ID NLM: 101623278

Informations de publication

Date de publication:
08 2020
Historique:
received: 11 02 2020
revised: 18 05 2020
accepted: 05 06 2020
entrez: 29 8 2020
pubmed: 29 8 2020
medline: 18 8 2021
Statut: ppublish

Résumé

Examine whether cognitive reserve moderates the association of 1) vascular risk factors and 2) white matter hyperintensity burden with risk of clinical progression and longitudinal cognitive decline. BIOCARD Study participants were cognitively normal and primarily middle-aged (M = 57 years) at baseline and have been followed with annual cognitive and clinical assessments (M = 13 years). Baseline cognitive reserve was indexed with a composite score combining education with reading and vocabulary scores. Baseline vascular risk (N = 229) was assessed with a composite risk score reflecting five vascular risk factors. Baseline white matter hyperintensity load (N = 271) was measured with FLAIR magnetic resonance imaging. Cox regression models assessed risk of progression from normal cognition to onset of clinical symptoms of Mild Cognitive Impairment. Longitudinal mixed effects models measured the relationship of these variables to cognitive decline, using a global composite score, and executive function and episodic memory sub-scores. Both vascular risk and white matter hyperintensities were associated with cognitive decline, particularly in executive function. Higher vascular risk, but not white matter hyperintensity burden, was associated with an increased risk of progression to Mild Cognitive Impairment. Higher cognitive reserve was associated with a reduced risk of symptom onset and higher levels of baseline cognition but did not modify the associations between the vascular risk score and white matter hyperintensities with clinical progression or cognitive decline. Although cognitive reserve has protective effects on clinical and cognitive outcomes, it does not mitigate the negative impact of vascular risk and small vessel cerebrovascular disease on these same outcomes.

Identifiants

pubmed: 32856790
doi: 10.1002/acn3.51120
pmc: PMC7448143
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1307-1317

Subventions

Organisme : NIA NIH HHS
ID : U19 AG033655
Pays : United States
Organisme : NIH HHS
ID : P50-AG005146
Pays : United States
Organisme : NIH HHS
ID : U19-AG033655
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG066507
Pays : United States
Organisme : NIH HHS
ID : K24-AG052573
Pays : United States

Informations de copyright

© 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Anja Soldan (A)

Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

Corinne Pettigrew (C)

Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

Yuxin Zhu (Y)

Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21287.

Mei-Cheng Wang (MC)

Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21287.

Rebecca F Gottesman (RF)

Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

Charles DeCarli (C)

Department of Neurology, University of California, Davis, School of Medicine, Davis, CA, 95616.

Marilyn Albert (M)

Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

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