4.5 Article

Patterns of progression of cerebral small vessel disease markers in older adults of Amerindian ancestry: a population-based, longitudinal prospective cohort study

期刊

AGING CLINICAL AND EXPERIMENTAL RESEARCH
卷 34, 期 11, 页码 2751-2759

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SPRINGER
DOI: 10.1007/s40520-022-02223-8

关键词

Cerebral small vessel disease; White matter hyperintensities; Cerebral microbleeds; Lacunes; Enlarged basal ganglia-perivascular spaces; Amerindians

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  1. Universidad Espiritu Santo-Ecuador

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The progression patterns of cerebral small vessel disease markers in older adults of Amerindian ancestry were found to be different from those in other races/ethnic groups. The independent progression of lacunes suggests different pathogenic mechanisms compared to other markers of cerebral small vessel disease.
Background Progression of cerebral small vessel disease (cSVD) markers has been studied in different races/ethnic groups. However, information from individuals of Amerindian ancestry is lacking. We sought to evaluate progression patterns of cSVD markers in community-dwelling older adults of Amerindian ancestry. Methods Following a longitudinal prospective study design, participants of the Atahualpa Project Cohort aged >= 60 years received a baseline brain MRI and clinical interviews. Those who also received a brain MRI at the end of the study were included. Poisson regression models were fitted to assess cSVD markers progression according to their baseline load after a median follow-up of 6.5 +/- 1.4 years. Logistic regression models were fitted to assess interrelations in the progression of the different cSVD markers at the end of the study. Results The study included 263 individuals (mean age: 65.7 +/- 6.2 years). Progression of white matter hyperintensities (WMH) was noticed in 103 (39%) subjects, cerebral microbleeds in 25 (12%), lacunes in 12 (5%), and enlarged basal ganglia-perivascular spaces (BG-PVS) in 56 (21%). Bivariate Poisson regression models showed significant associations between WMH severity at baseline and progression of WMH and enlarged BG-PVS. These associations became non-significant in multivariate models adjusted for clinical covariates. Logistic regression models showed interrelated progressions of WMH, cerebral microbleeds and enlarged BG-PVS. The progression of lacunes was independent. Conclusions Patterns of cSVD marker progression in this population of Amerindians are different than those reported in other races/ethnic groups. The independent progression of lacunes suggests different pathogenic mechanisms with other cSVD markers.

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