Cited by 209Neurological Disease Mechanisms and TreatmentsNitric Oxide and Endothelin EffectsDementia and Cognitive Impairment Research

Threats to the Mind: Aging, Amyloid, and Hypertension

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Iadecola, Costantino, Park, Laibaik, Capone, Carmen·2009·Stroke

Abstract

Aging, Alzheimer disease, and hypertension, major determinants of cognitive dysfunction, are associated with profound alterations in the structure and function of cerebral blood vessels. These vascular alterations may impair the delivery of energy substrates and nutrients to the active brain, and impede the clearance of potentially toxic metabolic byproducts. Reactive oxygen species derived form the enzyme NADPH oxidase are key pathogenic effectors of the cerebrovascular dysregulation. The resulting alterations in the homeostasis of the cerebral microenvironment may lead to cellular dysfunction and death and to cognitive impairment. The prominent role that cerebrovascular oxidative stress plays in conditions associated with cognitive impairment suggests new therapeutic opportunities to counteract and, possibly, reverse the devastating effects of cerebrovascular dysfunction on the brain.

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Crossref · 10.1161/strokeaha.108.533638

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  • The neurovascular unit is profoundly disrupted in vascular cognitive impairment and Alzheimer disease.

    “The neurovascular unit is profoundly disrupted in VCI and Alzheimer disease.95,100–103”

    From Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association (2011) · cites this paper as [102]

    The Alzheimer Disease section describes substantial structural and functional cerebrovascular abnormalities in AD. The Conclusions and “How Does Cerebrovascular Dysfunction Lead to Cognitive Deficits?” sections also link vascular and blood–brain barrier changes to cognitive deficits. The paper does not specifically discuss vascular cognitive impairment (VCI) as a condition or state that the neurovascular unit is profoundly disrupted in VCI. (LLM, conf=0.82)

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Authors
Iadecola, C., Park, L., & Capone, C.
Affiliations
Cornell University (US)
Venue
Stroke
Published
2009-03
Volume
40
Issue
3_suppl_1
Pages
S40-4
ISSN
  • 0039-2499 (ISSN-L)
  • 1524-4628
OpenAlex
W2068846977
Cited by
207
References
29
Citations by year
2026: 3 · 2025: 2 · 2024: 4 · 2023: 11 · 2022: 4 · 2021: 9 · 2020: 12 · 2019: 9 · 2018: 10 · 2017: 9 · 2016: 15 · 2015: 10 · 2014: 19 · 2013: 21 · 2012: 22
FWCI
10.29
Type
journal article
Language
en
Open access
Locations
  • Stroke (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (2r01ns038252-06)
  • National Heart, Lung, and Blood Institute (HL-18974, P01HL018974)
  • National Institute of Neurological Disorders and Stroke (NS-38252)
Topics
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
cerebrovascular dysfunction, cognitive impairment, Alzheimer's disease, aging, hypertension, cerebral vasculature, reactive oxygen species, NADPH oxidase, oxidative stress, neurodegeneration
MeSH terms
Aging, Alzheimer Disease, Amyloid, Cognition Disorders, Humans, Hypertension, Dementia, Vascular, Reactive Oxygen Species

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