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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.

Titel:	Impaired neurovascular coupling in aging and Alzheimer's disease: Contribution of astrocyte dysfunction and endothelial impairment to cognitive decline.
Autor/in / Beteiligte Person:	Tarantini, S ; Tran, CHT ; Gordon, GR ; Ungvari, Z ; Csiszar, A
Zeitschrift:	Experimental gerontology, Jg. 94 (2017-08-01), S. 52-58
Veröffentlichung:	Tarrytown Ny : Elsevier Science ; <i>Original Publication</i>: Oxford., 2017
Medientyp:	academicJournal
ISSN:	1873-6815 (electronic)
DOI:	10.1016/j.exger.2016.11.004
Schlagwort:	Age Factors Alzheimer Disease metabolism Alzheimer Disease pathology Alzheimer Disease psychology Animals Astrocytes metabolism Calcium Signaling Cellular Senescence Cerebrovascular Circulation Cognition Disorders metabolism Cognition Disorders pathology Cognition Disorders psychology Endothelium, Vascular metabolism Humans Insulin-Like Growth Factor I metabolism Microcirculation Oxidative Stress Alzheimer Disease physiopathology Astrocytes pathology Cognition Cognition Disorders physiopathology Cognitive Aging Endothelium, Vascular physiopathology Neurovascular Coupling
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Review; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural Language: English [Exp Gerontol] 2017 Aug; Vol. 94, pp. 52-58. <i>Date of Electronic Publication: </i>2016 Nov 12. MeSH Terms: Cognition* ; Cognitive Aging* ; Neurovascular Coupling* ; Alzheimer Disease / physiopathology ; Astrocytes / pathology ; Cognition Disorders / physiopathology ; Endothelium, Vascular / physiopathology ; Age Factors ; Alzheimer Disease / metabolism ; Alzheimer Disease / pathology ; Alzheimer Disease / psychology ; Animals ; Astrocytes / metabolism ; Calcium Signaling ; Cellular Senescence ; Cerebrovascular Circulation ; Cognition Disorders / metabolism ; Cognition Disorders / pathology ; Cognition Disorders / psychology ; Endothelium, Vascular / metabolism ; Humans ; Insulin-Like Growth Factor I / metabolism ; Microcirculation ; Oxidative Stress References: Life Sci. 2012 Oct 29;91(17-18):872-7. 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(PMID: 22451468) Grant Information: R01 AG038747 United States AG NIA NIH HHS; P30 AG050911 United States AG NIA NIH HHS; R01 AT006526 United States AT NCCIH NIH HHS; R01 NS056218 United States NS NINDS NIH HHS; P30 AG028718 United States AG NIA NIH HHS; T32 AG052363 United States AG NIA NIH HHS; Canada CIHR; R01 AG047879 United States AG NIA NIH HHS Contributed Indexing: Keywords: Cerebral circulation; Cerebrovascular; Functional hyperemia; Geroscience; Microcirculation; Neurovascular coupling; Senescence; VCI; VCID; Vascular aging Substance Nomenclature: 0 (IGF1 protein, human) ; 67763-96-6 (Insulin-Like Growth Factor I) Entry Date(s): Date Created: 20161116 Date Completed: 20180402 Latest Revision: 20220409 Update Code: 20240513 PubMed Central ID: PMC5429210

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Impaired neurovascular coupling in aging and Alzheimer's disease: Contribution of astrocyte dysfunction and endothelial impairment to cognitive decline.