ArticleThe Journal of experimental medicine2026
Amyloidosis of bridging veins is a pathologic feature of Alzheimer's disease.
Article in The Journal of experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Regional Cerebrospinal Fluid Motility as a Key Determinant of Soluble Amyloid-β Levels and Kinetics.Research square · 2026Article
- Article
- WSB.APP/PS1 mice develop age-dependent cerebral amyloid angiopathy, cerebrovascular dysfunction, and white matter deficits.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Astrocytic cholesterol jams brain clearance in AD.Nature neuroscience · 2026Article
- Engineering chimeric antigen receptor CD4 T cells for Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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Authors and funding
20 authors.
Funding
Abstract
Alzheimer's disease (AD) is characterized by the accumulation of extracellular aggregated amyloid beta, resulting from impaired waste clearance. We recently identified new cerebrospinal fluid (CSF) efflux structures termed arachnoid cuff exit (ACE) points and speculated that these may be impacted in AD, leading to impaired waste clearance function. Using 5XFAD mice, we found progressive amyloidosis of bridging veins at ACE points. Indeed, in 5XFAD mice, there is impaired CSF efflux to the dura mater, impaired CSF flow along bridging veins, and impaired blood flow through bridging veins. These observations suggest that ACE point amyloidosis plays a role in waste clearance dysfunction in AD. In postmortem human samples, we also found striking amyloidosis of the bridging veins of individuals with AD. Moreover, in human AD specimens, there was prominent bridging vein structural degeneration, indicating advanced pathology and stronger deficits in humans. We propose that bridging vein amyloidosis is an underrecognized pathophysiological correlate of AD that may impair CSF efflux, intracranial pressure, vascular reactivity, and vascular integrity.
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