期刊
EXPERIMENTAL GERONTOLOGY
卷 94, 期 -, 页码 52-58出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2016.11.004
关键词
Geroscience; Senescence; Vascular aging; Microcirculation; Cerebral circulation; Cerebrovascular; Functional hyperemia; Neurovascular coupling; VCID; VCI
资金
- American Heart Association
- National Center for Complementary and Alternative Medicine [R01-AT006526]
- National Institute on Aging [R01-AG047879, R01-AG038747, 3P30AG050911-02S1]
- National Institute of Neurological Disorders and Stroke (NINDS) [R01-NS056218]
- Arkansas Claude Pepper Older Americans Independence Center at University of Arkansas Medical Center [P30 AG028718]
- Oklahoma Center for the Advancement of Science and Technology
- Reynolds Foundation
- Canadian Institutes of Health Research
- Canada Research Chair
- Alberta Innovates Health Solutions
The importance of (micro)vascular contributions to cognitive impairment and dementia (VCID) in aging cannot be overemphasized, and the pathogenesis and prevention of age-related cerebromicrovascular pathologies are a subject of intensive research. In particular, aging impairs the increase in cerebral blood flow triggered by neural activation (termed neurovascular coupling or functional hyperemia), a critical mechanism that matches oxygen and nutrient delivery with the increased demands in active brain regions. From epidemiological, clinical and experimental studies the picture emerges of a complex functional impairment of cerebral microvessels and astrocytes, which likely contribute to neurovascular dysfunction and cognitive decline in aging and in age-related neurodegenerative diseases. This overview discusses age-related alterations in neurovascular coupling responses responsible for impaired functional hyperemia. The mechanisms and consequences of astrocyte dysfunction (including potential alteration of astrocytic endfeet calcium signaling, dysregulation of eicosanoid gliotransmitters and astrocyte energetics) and functional impairment of the microvascular endothelium are explored. Age related mechanisms (cellular oxidative stress, senescence, circulating IGF-1 deficiency) impairing the function of cells of the neurovascular unit are discussed and the evidence for the causal role of neurovascular uncoupling in cognitive decline is critically examined. (C) 2016 Elsevier Inc All rights reserved.
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