ArticleCirculation research2016
Loss of Endothelial Nitric Oxide Synthase Promotes p25 Generation and Tau Phosphorylation in a Murine Model of Alzheimer's Disease.
Article in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.The Journal of physiology · 2026Pooled it
- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- Dietary salt, vascular dysfunction, and cognitive impairment.Cardiovascular research · 2025Review
- The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Cerebrovascular Endothelial Dysfunction: Role of BACE1.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Peroxiredoxin 1 inhibits streptozotocin-induced Alzheimer's disease-like pathology in hippocampal neuronal cells via the blocking of CaScientific reports · 2024Article
- Pathogenic soluble tau peptide disrupts endothelial calcium signaling and vasodilation in the brain microvasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Constitutive NOS Production Is Modulated by Alzheimer's Disease Pathology Depending on APOE Genotype.International journal of molecular sciences · 2024Article
- The Impact of LY487379 or CDPPB on eNOS Expression in the Mouse Brain and the Effect of Joint Administration of Compounds with NOMolecules (Basel, Switzerland) · 2024Article
- BACE2 deficiency impairs expression and function of endothelial nitric oxide synthase in brain endothelial cells.Journal of neurochemistry · 2023Article
- Preserved endothelium-independent vascular function with aging in men and women: evidence from the peripheral and cerebral vasculature.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Article
- Hypertension and cognitive dysfunction: a narrative review.Journal of Yeungnam medical science · 2023Article
- CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
- Soluble pathogenic tau enters brain vascular endothelial cells and drives cellular senescence and brain microvascular dysfunction in a mouse model of tauopathy.Nature communications · 2023Article
- Review
- Inactivation of BACE1 increases expression of endothelial nitric oxide synthase in cerebrovascular endothelium.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Article
- Partial Endothelial Nitric Oxide Synthase Deficiency Exacerbates Cognitive Deficit and Amyloid Pathology in the APPswe/PS1ΔE9 Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAlzheimer's disease has an unknown pathogenesis; however, cardiovascular risk factors are associated with a higher incidence of Alzheimer's disease. A defining feature of endothelial dysfunction induced by cardiovascular risk factors is reduced bioavailable endothelial nitric oxide (NO). We previously demonstrated that endothelial NO acts as an important signaling molecule in neuronal tissue.
objectiveWe sought to determine the relationship between the loss of endothelial NO synthase (eNOS) and tau phosphorylation in neuronal tissue. METHODS AND
resultsWe used eNOS knockout (
conclusionsOur data suggests that loss of endothelial NO plays an important role in the generation of p25 and resulting tau phosphorylation in neuronal tissue. These findings provide important new insights into the molecular mechanisms linking endothelial dysfunction with the pathogenesis of Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.