ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Fibrillar tau alters cerebral endothelial cell metabolism, vascular inflammatory activation, and barrier function in vitro and in vivo.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Endothelial miR-15a/16-1 Regulation of SYNE1 Mediates Structural and Functional Recovery after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cerebrovascular Single-Nucleus RNA-Seq Reveals Heat Shock Activation and Vascular Remodeling in Alzheimer's Disease and Primary Tauopathies.Research square · 2026Article
- Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.Biomolecules · 2026Review
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- CSF Levels of Baseline VCAM-1 and ICAM-1 Are Associated with Tau Pathology in Patients Demonstrating Cognitive Impairment.Neurology international · 2026Article
- Contributions of vascular ageing to late-onset Alzheimer's disease.Experimental physiology · 2026Review
- Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Chronic cerebral hypoperfusion exacerbates amyloid and tau pathology by impairing glymphatic transport via AQP4- and VEGF-mediated pathways: insights from a vascular to mixed-type dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Article
- Modeling neurovascular dysfunction in Alzheimer's disease using an isogenic brain-chip model.Fluids and barriers of the CNS · 2026Article
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- CSF markers of vascular injury correlate with tau and cognitive decline in early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Astrocyte-driven vasoconstriction impairs glymphatic clearance in a human tauopathy-on-chip model.APL bioengineering · 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
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- How endothelial cell metabolism shapes blood-brain barrier integrity in neurodegeneration.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
introductionThe presence of tau aggregates in and around the brain vasculature in Alzheimer's disease (AD) and tauopathies suggests its possible pathogenicity to cerebral endothelial cells (ECs).
methodsWe used an in vitro model of the blood-brain barrier (BBB) to understand the mechanisms of fibrillar tau-mediated cerebral EC and BBB pathology, confirming our findings in 3-month-old P301S mice brains and extracted microvessels.
resultsProtofibrillar and fibrillar tau species induce endothelial barrier permeability through an increase in glycolysis, which activates ECs toward a pro-inflammatory phenotype, inducing loss of junction protein expression and localization. The Warburg-like metabolic shift toward glycolysis and increased vascular pathological phenotypes are also present in young P301S mice. DISCUSSION: In sum, our work reveals that fibrillar tau species, by enhancing endothelial glycolytic metabolism, promote vascular inflammatory phenotypes and loss of BBB function, highlighting the importance of addressing and targeting early tau-mediated neurovascular damage in AD and tauopathies. HIGHLIGHTS: We improve the understanding of the mechanisms of vascular pathology in tauopathies. Fibrillar tau mediates vascular metabolic changes, inflammation, and blood-brain barrier (BBB) dysfunction. These events are replicated at early stages in a tauopathy mouse model. Inhibiting altered glycolysis reduces BBB permeability and endothelial activation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.