Abstract
Alzheimer’s disease (AD) and related dementias disproportionately impact racial and ethnic minorities. The racial and ethnic disparities in AD could be explained by differences in cerebral vascular disease pathology. Endothelin-1 (ET-1) is a potent vasoconstrictive peptide that regulates smooth muscle, endothelial cell, and pericyte contractions that may result in cerebral vascular constriction, leading to cerebral hypoperfusion; over time, ET-1 may result in neuronal injury contributing to the pathology of AD. Upregulation of the ET-1 system has been observed in African Americans when compared with non-Hispanic Whites. The role of the ET-1 system as a driver of ethnic disparities in AD requires further investigation. Targeting of the ET-1 system as a therapeutic intervention that could impact AD progression also needs further study. Dysregulation of ET-1 in Hispanic/Latino populations largely have been unexplored. Genetics linking ET-1 dysregulation and racial disparities in AD also needs further investigation. In this review, I examine how AD effects underserved minority populations and how dysregulation of the ET-1 system specifically predisposes ethnic minorities to AD. In addition, I examine the molecular interactions of the ET-1 system and amyloid beta, the role the ET-1 system in neurodegeneration, potential therapeutics for ET-1 dysregulation, and the impact on AD progression.
Highlights
Underserved Minority Populations and Alzheimer’s disease (AD)Regardless of the health disparities associated with AD among ethnic minorities, large population-based studies that examined the pathobiology of AD have been performed with predominantly non-Hispanic Whites (NHWs), resulting in extrapolation of research findings to minority populations [17,18]
Alzheimer’s disease (AD) and related dementias disproportionately impact racial and ethnic minorities
These findings suggest that AAs are at higher risk for cardiovascular disease than non-Hispanic Whites (NHWs), which increases their risk of dementia
Summary
Regardless of the health disparities associated with AD among ethnic minorities, large population-based studies that examined the pathobiology of AD have been performed with predominantly NHWs, resulting in extrapolation of research findings to minority populations [17,18]. Aging and genetics are important risk factors; other demographic factors in the United States (U.S.) are rising for AD, including a surge in Hispanic/Latino (H/L) populations [19,20]. Vega et al examined the interplay between social determinants of health, co-morbidities, and genetic factors associated with AD in H/L communities [28]. While the burden of U.S disparities in AD is associated directly with social disparities, racial and ethnic disparities could be explained in part by differences in susceptibility to vascular disease
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