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You Are as Old as Your Arteries ‐ And Microvessels
Author(s) -
Ungvari Zoltan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.11.3
Subject(s) - neurovascular bundle , medicine , endothelial dysfunction , microcirculation , stroke (engine) , disease , endothelium , cerebral blood flow , cardiology , neuroscience , pathology , psychology , mechanical engineering , engineering
Nearly four centuries ago the famous English physician Thomas Sydenham (1624‐1689) commented that “a man is as old as his arteries.” Cardiovascular diseases are the indeed most common cause of death among the elderly patients in the Western world. It is becoming evident that aging results in well‐defined phenotypic changes, which render the cardiovascular system prone to disease even in the absence of traditional risk factors. The consequences of vascular aging range from myocardial infarction through erectile dysfunction to stroke. In addition to its deleterious effects on large arteries aging also results in functional and phenotypic alterations at the level of the microcirculation. There is increasing evidence that age‐related microvascular impairment plays a critical role in the pathogenesis of vascular cognitive impairment (VCI). The potential roles of microvascular mechanisms involved in VCI, including microvascular rarefaction and disruption of the blood‐brain barrier will be discussed. Also, moment‐to‐moment adjustment of cerebral blood flow via neurovascular coupling is essential for the maintenance of normal neuronal function. Increased oxidative stress that occurs with aging was shown to impair neurovascular coupling, which likely contributes to a significant age‐related decline in higher cortical function, increasing the risk for VCI. There are suggestions in the literature and new data will be presented that in aged laboratory rodents neurovascular coupling and endothelium‐dependent cerebromicrovascular dilation can be rescued, which represents a potential therapeutic target for the promotion of healthy brain aging.