ArticleActa neuropathologica2024
Brain vasculature accumulates tau and is spatially related to tau tangle pathology in Alzheimer's disease.
Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Cerebrovascular Single-Nucleus RNA-Seq Reveals Heat Shock Activation and Vascular Remodeling in Alzheimer's Disease and Primary Tauopathies.Research square · 2026Article
- Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease.Alzheimer's research & therapy · 2026Article
- Peripheral vascular function, including endothelium-dependent measures, and dementia risk: The Framingham Heart Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Contributions of vascular ageing to late-onset Alzheimer's disease.Experimental physiology · 2026Review
- Post-mortem evidence of pathogenic angiogenesis and abnormal vascular function in early Alzheimer's disease.Brain : a journal of neurology · 2026Article
- VesSynth: Tubes Are All You Need for Robust Cross-Scale Cross-Modal 3D Vessel Segmentation.bioRxiv : the preprint server for biology · 2026Article
- Vascular β-amyloid potentially colocalises with phosphorylated tau in cerebral amyloid angiopathy.Stroke and vascular neurology · 2026Article
- Circulating C-reactive protein influences polygenic risk of inflammatory genes expressed in brain endothelia for Alzheimer's disease.Neurobiology of disease · 2026Article
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Impact of APOE on cerebrovascular lipid profile in Alzheimer's disease.Acta neuropathologica · 2025Article
- Lead-induced hypertension and cognitive dysfunction: brain amyloid pathology.European journal of medical research · 2025Article
- Lipid mediated formation of antiparallel aggregates in cerebral amyloid angiopathy.Acta neuropathologica · 2025Article
- Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Perivascular brain clearance as a therapeutic target in cerebral amyloid angiopathy and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- 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
- The influences of ApoE isoforms on endothelial adherens junctions and actin cytoskeleton responding to mCRP.Angiogenesis · 2024Article
- Molecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Molecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.Frontiers in neurology · 2024Article
Corrections and comments
- Update of
Authors and funding
9 authors.
Funding
Abstract
Insoluble pathogenic proteins accumulate along blood vessels in conditions of cerebral amyloid angiopathy (CAA), exerting a toxic effect on vascular cells and impacting cerebral homeostasis. In this work, we provide new evidence from three-dimensional human brain histology that tau protein, the main component of neurofibrillary tangles, can similarly accumulate along brain vascular segments. We quantitatively assessed n = 6 Alzheimer's disease (AD), and n = 6 normal aging control brains and saw that tau-positive blood vessel segments were present in all AD cases. Tau-positive vessels are enriched for tau at levels higher than the surrounding tissue and appear to affect arterioles across cortical layers (I-V). Further, vessels isolated from these AD tissues were enriched for N-terminal tau and tau phosphorylated at T181 and T217. Importantly, tau-positive vessels are associated with local areas of increased tau neurofibrillary tangles. This suggests that accumulation of tau around blood vessels may reflect a local clearance failure. In sum, these data indicate that tau, like amyloid beta, accumulates along blood vessels and may exert a significant influence on vasculature in the setting of AD.
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.