Key result
Microvascular impairment and oxidative stress drive vascular cognitive impairment by disrupting neurovascular coupling.
Why the study?
Aging causes functional and phenotypic alterations in the microcirculation, and increasing evidence indicates that age-related microvascular impairment and impaired neurovascular coupling play a critical role in the pathogenesis of vascular cognitive impairment.
Hypothesis-generating for oxidative stress-targeted rescue in vascular cognitive impairment; prospective human trials needed before clinical adoption.
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.
No takes yet. Share an insight, caveat, or question.
Zoltan I. Ungvari (2015) conducted a review in Vascular cognitive impairment and cardiovascular aging. Age-related microvascular impairment and oxidative stress was evaluated on Neurovascular coupling and vascular cognitive impairment. Age-related microvascular impairment and oxidative stress impair neurovascular coupling and promote vascular cognitive impairment, though rescues are possible in aged rodent models.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: