Soluble epoxide hydrolase drives neurovascular dysfunction in a model of amyloidosis

Clicks: 17
ID: 314649
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #355 of 457 articles by views in Brain research

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 457 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Recent advances in anti-amyloid therapies for Alzheimer's disease have been promising, but they have also highlighted critical challenges, including increased vascular complications, such as amyloid-related imaging abnormalities. Emerging evidence suggests that the soluble epoxide hydrolase may be a promising therapeutic target due to the involvement of sEH-derived diols in inflammation, oxidative stress, and vascular destabilization. APPPS1 mice, a model of amyloidosis, were crossed with an inducible soluble epoxide hydrolase knock-out mouse line. The knock-out was induced before onset of amyloid deposition, and then the mice were analyzed using histological, molecular, and RNA sequencing techniques. Here, we identify astrocytic soluble epoxide hydrolase as a key mediator of vascular instability in amyloid pathology. Targeted astrocyte-specific deletion of soluble epoxide hydrolase in APPPS1 mice dramatically mitigated vascular changes, reducing the vascular amyloid burden by 67.95% and preserving VE-cadherin architecture. Importantly, vasomotion was markedly impaired in the Alzheimer's disease model and was preserved in soluble epoxide hydrolase-deficient animals. Transcriptomic profiling of vasculature in APPPS1xsEHΔAC mice revealed upregulated expression of genes critical for neurovascular protection. These findings identify soluble epoxide hydrolase as a central regulator of neurovascular dysfunction and underscore its therapeutic potential in increasing vascular stability in amyloidosis-associated diseases, such as Alzheimer's disease.
Reference Key
openalex_W7162079525 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Murphy DeMeglio, Eloah S. De Biasi, Peter Breunig, Michael Candlish, Christina Sauerland, Stefan Günther, Haruya Kawase, Blanca Peguera, Christine Bohnstaedt, Jochen Herms, AS Neubauer, Jonas J. Neher, Peter R. Nilsson, Jiong Hu, Susanne Hille, Oliver Müller, Amparo Acker‐Palmer, Bruce D Hammock, T Michael Underhill, Stephan Junek, Stefan Offermanns, Ingrid Fleming, Jasmin K. Hefendehl
Are you one of these authors? Claim your profile
Journal Brain research
Year 2026
DOI
10.1093/brain/awag184
URL
https://doi.org/10.1093/brain/awag184
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.