期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 312, 期 6, 页码 H1128-H1143出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00780.2016
关键词
vascular contributors to cognitive impairment and dementia; vascular cognitive impairment; vascular aging; cerebrovascular; cerebromicrovascular; stroke; transient ischemic attack
资金
- American Heart Association
- National Institutes of Health (NIH) [R01-AT-006526, R01-AG-047879, R01-AG-038747, U54-GM-104938, R01-NS-056218]
- Oklahoma Nathan Shock Center (NIH) [3-P30-AG-050911-02S1]
- Arkansas Claude Pepper Older Americans Independence Center at University of Arkansas Medical Center (NIH) [P30-AG-028718]
- Oklahoma Center for the Advancement of Science and Technology
- Oklahoma IDeA Network for Biomedical Research Excellence
- Department of Veterans Affairs [CX000340]
- Reynolds Foundation
The increasing prevalence of multifocal cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) is a significant, newly recognized problem in the aging population of the Western world. CMHs are associated with rupture of small intracerebral vessels and are thought to progressively impair neuronal function, potentially contributing to cognitive decline, geriatric psychiatric syndromes, and gait disorders. Clinical studies show that aging and hypertension significantly increase prevalence of CMHs. CMHs are also now recognized by the National Institutes of Health as a major factor in Alzheimer's disease pathology. Moreover, the presence of CMHs is an independent risk factor for subsequent larger intracerebral hemorrhages. In this article, we review the epidemiology, detection, risk factors, clinical significance, and pathogenesis of CMHs. The potential age-related cellular mechanisms underlying the development of CMHs are discussed, with a focus on the structural determinants of microvascular fragility, age-related alterations in cerebrovascular adaptation to hypertension, the role of oxidative stress and matrix metalloproteinase activation, and the deleterious effects of arterial stiffening, increased pulse pressure, and impaired myogenic autoregulatory protection on the brain microvasculature. Finally, we examine potential treatments for the prevention of CMHs based on the proposed model of agingand hypertension-dependent activation of the reactive oxygen species-matrix metalloproteinases axis, and we discuss critical questions to be addressed by future studies.
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