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Healthcare 2015, 3(2), 233-251; doi:10.3390/healthcare3020233

NADPH Oxidase Activity in Cerebral Arterioles Is a Key Mediator of Cerebral Small Vessel Disease—Implications for Prevention

Catalytic Longevity, 7831 Rush Rose Dr., Apt 316, Carlsbad, CA 92009, USA
Academic Editors: Samir Samman and Ian Darnton-Hill
Received: 1 December 2014 / Revised: 21 March 2015 / Accepted: 8 April 2015 / Published: 15 April 2015
(This article belongs to the Special Issue The Close Relationship: Health and Nutrition)
View Full-Text   |   Download PDF [579 KB, uploaded 15 April 2015]   |  

Abstract

Cerebral small vessel disease (SVD), a common feature of brain aging, is characterized by lacunar infarcts, microbleeds, leukoaraiosis, and a leaky blood-brain barrier. Functionally, it is associated with cognitive decline, dementia, depression, gait abnormalities, and increased risk for stroke. Cerebral arterioles in this syndrome tend to hypertrophy and lose their capacity for adaptive vasodilation. Rodent studies strongly suggest that activation of Nox2-dependent NADPH oxidase activity is a crucial driver of these structural and functional derangements of cerebral arterioles, in part owing to impairment of endothelial nitric oxide synthase (eNOS) activity. This oxidative stress may also contribute to the breakdown of the blood-brain barrier seen in SVD. Hypertension, aging, metabolic syndrome, smoking, hyperglycemia, and elevated homocysteine may promote activation of NADPH oxidase in cerebral arterioles. Inhibition of NADPH oxidase with phycocyanobilin from spirulina, as well as high-dose statin therapy, may have potential for prevention and control of SVD, and high-potassium diets merit study in this regard. Measures which support effective eNOS activity in other ways—exercise training, supplemental citrulline, certain dietary flavonoids (as in cocoa and green tea), and capsaicin, may also improve the function of cerebral arterioles. Asian epidemiology suggests that increased protein intakes may decrease risk for SVD; conceivably, arginine and/or cysteine—which boosts tissue glutathione synthesis, and can be administered as N-acetylcysteine—mediate this benefit. Ameliorating the risk factors for SVD—including hypertension, metabolic syndrome, hyperglycemia, smoking, and elevated homocysteine—also may help to prevent and control this syndrome, although few clinical trials have addressed this issue to date. View Full-Text
Keywords: cerebral small vessel disease; NADPH oxidase; Nox2; eNOS; spirulina; potassium; arginine; cysteine; hypertension cerebral small vessel disease; NADPH oxidase; Nox2; eNOS; spirulina; potassium; arginine; cysteine; hypertension
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

McCarty, M.F. NADPH Oxidase Activity in Cerebral Arterioles Is a Key Mediator of Cerebral Small Vessel Disease—Implications for Prevention. Healthcare 2015, 3, 233-251.

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