ReviewBiomolecules2023
Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?
Review in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Treatment of Clinically Diagnosed Alzheimer's Disease by External Counterpulsation A Randomized Clinical Trial.American journal of Alzheimer's disease and other dementiasTrial
- Longitudinal effects of cerebrovascular reactivity and cerebral pulsatility in cognitively intact older adults with APOE4: links with cognition.GeroScience · 2026Article
- Glycation at the Gate: A Brain Endothelial Glycocalyx Model and Therapeutic Roadmap for Alzheimer's Disease.Biomedicines · 2026Article
- FOXO family and neurodegenerative diseases: Mechanisms of action and therapeutic potential.Redox biology · 2026Review
- Evolution of Multitarget Strategies for Alzheimer's Disease: From Cholinergic Inhibition to Network-Oriented Therapeutic Design (2006-2025).Pharmaceuticals (Basel, Switzerland) · 2026Article
- Time-restricted feeding rejuvenates cerebrovascular function and preserves cognition during aging.Research square · 2026Article
- Elevated levels of circulating plasma sPDGFRβ in cognitively impaired APOE4 carriers.GeroScience · 2026Article
- Multiple sevoflurane exposures in early development lead to long-term vascular abnormalities in the hippocampus.Cell biology and toxicology · 2026Article
- Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease.Alzheimer's research & therapy · 2026Article
- Dysfunctional astrocytes regulate excitatory neurons via cell adhesion and vascular lesions in patients with Alzheimer's disease.Journal of translational medicine · 2026Article
- Article
- Hypertension as a Major Risk Factor in Alzheimer's Disease: Mechanisms, Interactions and Therapeutic Perspectives.Clinical interventions in aging · 2026Review
- White matter hyperintensity modulates the amyloid-tau-cognition association and anti-amyloid treatment efficacy in asymptomatic older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Rapid amyloid-β clearance and cognitive recovery through multivalent modulation of blood-brain barrier transport.Signal transduction and targeted therapy · 2025Article
- Fibrillar tau alters cerebral endothelial cell metabolism, vascular inflammatory activation, and barrier function in vitro and in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Organelle stresses and energetic metabolisms promote endothelial-to-mesenchymal transition and fibrosis via upregulating FOSB and MEOX1 in Alzheimer's disease.Frontiers in molecular neuroscience · 2025Article
- The AβFrontiers in cellular neuroscience · 2024Article
- Article
- Cerebrovascular reactivity and plasma p-tau181 in Alzheimer's disease: Insights into APOE-related vascular phenotypes.Alzheimer's & dementia (New York, N. Y.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer disease (AD) models are based on the notion that abnormal protein aggregation is the primary event in AD, which begins a decade or longer prior to symptom onset, and culminates in neurodegeneration; however, emerging evidence from animal and clinical studies suggests that reduced blood flow due to capillary loss and endothelial dysfunction are early and primary events in AD pathogenesis, which may precede amyloid and tau aggregation, and contribute to neuronal and synaptic injury via direct and indirect mechanisms. Recent data from clinical studies suggests that endothelial dysfunction is closely associated with cognitive outcomes in AD and that therapeutic strategies which promote endothelial repair in early AD may offer a potential opportunity to prevent or slow disease progression. This review examines evidence from clinical, imaging, neuropathological, and animal studies supporting vascular contributions to the onset and progression of AD pathology. Together, these observations support the notion that the onset of AD may be primarily influenced by vascular, rather than neurodegenerative, mechanisms and emphasize the importance of further investigations into the vascular hypothesis of AD.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.