Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 320, Issue 2, Pages H740-H761Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00736.2020
Keywords
aging; endothelial dysfunction; metabolic syndrome; senescence
Funding
- Oklahoma Center for the Advancement of Science and Technology
- National Institute on Aging (NIA) [R01-AG047879, R01-AG038747, R01-AG055395, R01-AG068295]
- National Institute of Neurological Disorders and Stroke [R01-NS056218, R01-NS100782]
- National Institute of General Medical Sciences Oklahoma Shared Clinical and Translational Resources [GM104938]
- Presbyterian Health Foundation
- Oklahoma Nathan Shock Center [P30AG050911]
- Cellular and Molecular GeroScience CoBRE [1P20GM125528, 5337]
- NIA [T32AG052363]
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Over two-thirds of individuals aged 65 and older in the United States are obese or overweight, with an association between adiposity and cognitive dysfunction. This review discusses the pathophysiological roles of microvascular mechanisms in cognitive impairment in geriatric obesity.
Over two-thirds of individuals aged 65 and older are obese or overweight in the United States. Epidemiological data show an association between the degree of adiposity and cognitive dysfunction in the elderly. In this review, the pathophysiological roles of microvascular mechanisms, including impaired endothelial function and neurovascular coupling responses, microvascular rarefaction, and blood-brain barrier disruption in the genesis of cognitive impairment in geriatric obesity are considered. The potential contribution of adipose-derived factors and fundamental cellular and molecular mechanisms of senescence to exacerbated obesity-induced cerebromicrovascular impairment and cognitive decline in aging are discussed.
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