Interaction Between Arteriosclerosis and -β on Cognitive Function.

Alzheimer’s disease amyloid-β arteriosclerosis calcification dementia plasma biomarkers

Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
05 Jan 2024
Historique:
medline: 13 1 2024
pubmed: 13 1 2024
entrez: 13 1 2024
Statut: aheadofprint

Résumé

Dementia is a multifactorial disease, with Alzheimer's disease (AD) and vascular pathology often co-occurring in many individuals with dementia. Yet, the interplay between AD and vascular pathology in cognitive decline is largely undetermined. The aim of the present study was to examine the joint effect of arteriosclerosis and AD pathology on cognition in the general population without dementia. We determined the interaction between blood-based AD biomarkers and CT-defined arteriosclerosis on cognition in 2,229 dementia-free participants of the population-based Rotterdam Study (mean age: 68.9 years, 52% women) cross-sectionally. Amyloid-β (Aβ)42 and arterial calcification were associated with cognitive performance. After further adjustment for confounders in a model that combined all biomarkers, only arterial calcification remained independently associated with cognition. There was a significant interaction between arterial calcification and Aβ 42 and between arterial calcification and the ratio of Aβ 42/40. Yet, estimates attenuated, and interactions were no longer statistically significant after adjustment for cardio metabolic risk factors. Arteriosclerosis and AD display additive interaction-effects on cognition in the general population, that are due in part to cardio metabolic risk factors. These findings suggest that joint assessment of arteriosclerosis and AD pathology is important for understanding of disease etiology in individuals with cognitive impairment.

Sections du résumé

BACKGROUND BACKGROUND
Dementia is a multifactorial disease, with Alzheimer's disease (AD) and vascular pathology often co-occurring in many individuals with dementia. Yet, the interplay between AD and vascular pathology in cognitive decline is largely undetermined.
OBJECTIVE OBJECTIVE
The aim of the present study was to examine the joint effect of arteriosclerosis and AD pathology on cognition in the general population without dementia.
METHODS METHODS
We determined the interaction between blood-based AD biomarkers and CT-defined arteriosclerosis on cognition in 2,229 dementia-free participants of the population-based Rotterdam Study (mean age: 68.9 years, 52% women) cross-sectionally.
RESULTS RESULTS
Amyloid-β (Aβ)42 and arterial calcification were associated with cognitive performance. After further adjustment for confounders in a model that combined all biomarkers, only arterial calcification remained independently associated with cognition. There was a significant interaction between arterial calcification and Aβ 42 and between arterial calcification and the ratio of Aβ 42/40. Yet, estimates attenuated, and interactions were no longer statistically significant after adjustment for cardio metabolic risk factors.
CONCLUSIONS CONCLUSIONS
Arteriosclerosis and AD display additive interaction-effects on cognition in the general population, that are due in part to cardio metabolic risk factors. These findings suggest that joint assessment of arteriosclerosis and AD pathology is important for understanding of disease etiology in individuals with cognitive impairment.

Identifiants

pubmed: 38217596
pii: JAD230604
doi: 10.3233/JAD-230604
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

Ingeborg Frentz (I)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.
Department of Neurology, UMCG, Groningen, The Netherlands.

Joyce van Arendonk (J)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.
Department of Radiology & Nuclear Medicine, Erasmus MC, GD Rotterdam, The Netherlands.

Anna E Leeuwis (AE)

Alzheimer Center Amsterdam,Department of Neurology, Amsterdam Neuroscience,Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.

Meike W Vernooij (MW)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.
Department of Radiology & Nuclear Medicine, Erasmus MC, GD Rotterdam, The Netherlands.

Wiesje M van der Flier (WM)

Alzheimer Center Amsterdam,Department of Neurology, Amsterdam Neuroscience,Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Department of Epidemiology,Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.

Daniel Bos (D)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.
Department of Radiology & Nuclear Medicine, Erasmus MC, GD Rotterdam, The Netherlands.

Peter Paul De Deyn (PP)

Department of Neurology, UMCG, Groningen, The Netherlands.
Alzheimer Centre Groningen, UMCG, Groningen, The Netherlands.

Frank J Wolters (FJ)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.
Department of Radiology & Nuclear Medicine, Erasmus MC, GD Rotterdam, The Netherlands.

M Arfan Ikram (MA)

Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands.

Classifications MeSH