Abstract
Subclinical cerebrovascular disease is frequently identified in neuroimaging studies and is thought to play a role in the pathogenesis of cognitive disorders. Identifying the etiologies of different types of lesions may help investigators differentiate between age-related and pathological cerebrovascular damage in cognitive aging. In this review article, we aim to describe the epidemiology and etiology of various brain magnetic resonance imaging (MRI) measures of vascular damage in cognitively normal, older adult populations. We focus here on population-based prospective cohort studies of cognitively unimpaired older adults, as well as discuss the heterogeneity of MRI findings and their relationships with cognition. This review article emphasizes the need for a better understanding of subclinical cerebrovascular disease in cognitively normal populations, in order to more effectively identify and prevent cognitive decline in our rapidly aging population.
Highlights
Recent advancements in medicine, global health, and biotechnology have led to prolonged life expectancy, and a rapidly aging population (Ortman et al, 2014)
We can improve our understanding of cognitive aging by distinguishing between changes in magnetic resonance imaging (MRI) that are associated with normal vs. abnormal cognitive performance
The Rotterdam Study found that silent thalamic infarcts were associated with steeper declines in memory performance, while nonthalamic infarcts were related to steeper declines in psychomotor speed (Vermeer et al, 2003). These studies are limited in terms of racial and ethnic diversity, which decreases their generalizability to the U.S Overall, lacunar infarcts appear to be an important contributor to vascular cognitive impairment in populationbased elderly cohorts, but more work is warranted to examine cognitive performance in non-demented elderly, especially in racial/ethnic minorities who are at higher risk for developing dementia and vascular disease compared to non-Hispanic whites
Summary
Global health, and biotechnology have led to prolonged life expectancy, and a rapidly aging population (Ortman et al, 2014). Neuroimaging features of CSVD include small subcortical infarcts and lacunes, white matter hyperintensities (WMH) on MRI (hypodensities on computed tomography), prominent perivascular spaces, cerebral microbleeds (CMBs), disruption of the blood-brain barrier (BBB), Neuroimaging of CSVD and Cognition and diffusion-based markers of microstructural integrity (Alexander et al, 2007; Farrall and Wardlaw, 2009; Pantoni, 2010; Wardlaw et al, 2013b) These pathological entities form part of the American Heart Association (AHA)/American Stroke Association (ASA) definition of vascular contributions to cognitive impairment and dementia (VCID; Gorelick et al, 2011) and have been proposed as additions to recently published criteria for Alzheimer’s disease (Sweeney et al, 2019). The goal of this review article is to inform future research in age-related cognitive decline, better differentiate between normal and pathological brain aging, and generate hypotheses for how CSVD may contribute to normal and pathological cognitive aging
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