Emerging Roles of Endothelial Nitric Oxide in Preservation of Cognitive Health
Open accessAbstract
eNOS (endothelial nitric oxide synthase) is critically important enzyme responsible for regulation of cardiovascular homeostasis. Under physiological conditions, constitutive eNOS activity and production of endothelial nitric oxide (NO) exert essential neurovascular protective functions. In this review, we first discuss the roles of endothelial NO in prevention of neuronal amyloid accumulation and formation of neurofibrillary tangles, hallmarks of Alzheimer disease pathology. Next, we review existing evidence suggesting that NO released from endothelium prevents activation of microglia, stimulates glycolysis in astrocytes, and increases biogenesis of mitochondria. We also address major risk factors for cognitive impairment including aging and ApoE4 (apolipoprotein 4) genotype with focus on their detrimental effects on eNOS/NO signaling. Relevant to this review, recent studies suggested that aged eNOS heterozygous mice are unique model of spontaneous cerebral small vessel disease. In this regard, we review contribution of dysfunctional eNOS to deposition of Aβ (amyloid-β) into blood vessel wall leading to development of cerebral amyloid angiopathy. We conclude that endothelial dysfunction manifested by the loss of neurovascular protective functions of NO may significantly contribute to development of cognitive impairment.
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Endothelial primary cilia are shear-stress mechanosensors that regulate NO bioavailability, barrier integrity, and neurovascular coupling.
“recent reports also implicate endothelial primary cilia as shear-stress mechanosensors that regulate NO bioavailability, barrier integrity, and neurovascular coupling; work in AD models and patient-relevant systems associates endothelial cilia dysfunction with early neurovascular decoupling and cerebrovascular instability [52,55,56].”
From Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease (2025) · cites this paper as [56]
The 'Endothelial NO and Aβ cytotoxicity' section says shear stress stimulates eNOS expression, and the Conclusions link endothelial NO to blood–brain barrier permeability. The 'Nitric oxide in the cerebrovascular endothelium' section also describes NO-mediated communication between blood vessels and neurons. But the paper does not identify endothelial primary cilia as shear-stress sensors or attribute any of these effects to cilia. (LLM, conf=0.78)
Experimental — accuracy not yet measuredEndothelial cilia dysfunction is associated with early neurovascular decoupling and cerebrovascular instability in AD models and patient-relevant systems.
“work in AD models and patient-relevant systems associates endothelial cilia dysfunction with early neurovascular decoupling and cerebrovascular instability [52,55,56].”
From Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease (2025) · cites this paper as [56]
The 'Endothelial NO and Aβ cytotoxicity' section discusses cerebrovascular dysfunction in Alzheimer’s disease, but attributes it to amyloid-β and impaired nitric-oxide signaling, not endothelial cilia. Searches for cilia, neurovascular decoupling, and related terms found no passage linking cilia dysfunction to the claimed outcomes in AD models or patient-relevant systems. Page numbers are unavailable in our copy. (LLM, conf=0.76)
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Hypertension: Causes and Consequences of Circadian Rhythms in Blood Pressure
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Emerging diagnostic biomarkers and therapeutic targets in Alzheimer's disease
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Aging and Bioenergetics of Mitochondria
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Mapping the Nitric Oxide Axis in IVF: Genotype Associations in Antagonist Cycles
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Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression
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- Authors
- Katusic, Z. S., d’Uscio, L. V., & He, T.
- Affiliations
- Department of Anesthesiology and Perioperative Medicine (Z.S.K., L.V.d., T.H.), Mayo Clinic, Rochester, MN.
- Mayo Clinic (US)
- Venue
- Stroke
- Published
- 2023-03
- Volume
- 54
- Issue
- 3
- Pages
- 686-696
- ISSN
- 0039-2499 (ISSN-L)
- 1524-4628
- PMC
- PMC9991080
- OpenAlex
- W4322490498
- Cited by
- 73
- References
- 117
- Citations by year
- 2026: 13 · 2025: 27 · 2024: 21 · 2023: 12
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Stroke (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG071190)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- endothelial nitric oxide, endothelial nitric oxide synthase, Alzheimer's disease, amyloid-beta, neurofibrillary tangles, microglial activation, mitochondrial biogenesis, cognitive impairment, aging, APOE ε4, cerebral small vessel disease, cerebral amyloid angiopathy, endothelial dysfunction, neurovascular protection
- MeSH terms
- Aging, Alzheimer Disease, Animals, Cognition, Endothelium, Nitric Oxide, Mice
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