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      Impaired neurovascular coupling in aging and Alzheimer’s disease: contribution of astrocyte dysfunction and endothelial impairment to cognitive decline

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          Abstract

          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.

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          Author and article information

          Journal
          0047061
          3650
          Exp Gerontol
          Exp. Gerontol.
          Experimental gerontology
          0531-5565
          1873-6815
          17 March 2017
          12 November 2016
          August 2017
          01 August 2018
          : 94
          : 52-58
          Affiliations
          [1 ]Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK
          [2 ]Hotchkiss Brain Institute, Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
          Author notes
          Correspondence: Anna Csiszar M.D., Ph.D., Reynolds Oklahoma Center on Aging, University of Oklahoma HSC, 975 NE 10 th Street, BRC 1311, Oklahoma City, OK 73104, USA, anna-csiszar@ 123456ouhsc.edu
          Article
          PMC5429210 PMC5429210 5429210 nihpa834079
          10.1016/j.exger.2016.11.004
          5429210
          27845201
          9008cf1f-3f7c-4fa4-88c6-ef491237cb0b
          Categories
          Article

          microcirculation,VCI,VCID,neurovascular coupling,functional hyperemia,cerebrovascular,cerebral circulation,vascular aging,senescence,geroscience

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