ArticleStroke2025
Experimental Ischemic Stroke-Induced Alpha-Synuclein Pathology Enhances Endothelial Inflammatory Response and Impairs Angiogenesis.
Article in Stroke, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- von Willebrand Factor fibers formed at pathological high shear provide a scaffold for α-synuclein binding and aggregation.Scientific reports · 2026Article
- Beyond wound closure: translational opportunities and barriers of mesenchymal stem cells and their extracellular vesicles in burn management.Frontiers in cell and developmental biology · 2026Review
- Central Neurobiological Mechanisms of Acupuncture in Post-Stroke Depression: Multi-Target and Network-Based Regulation.Neuropsychiatric disease and treatment · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundα-Syn (alpha-synuclein) increases and oligomerization contributes to ischemic brain damage. Nevertheless, the exact mechanisms of ischemia-induced α-Syn pathology after stroke are understudied. In this exploratory and hypothesis-testing study, we specifically investigated how ischemia-induced α-Syn pathology impacts vascular inflammation and angiogenesis.
methodsTransient focal cerebral ischemia was induced in C57BL/6J wild-type and C57BL/6S mice with spontaneous deletion of α-Syn. In total, 72 mice were randomized to receive sham (12) or ischemia (60), with 1:1 allocation to genotype. Ischemic mice were included if presenting ≥3 intraischemic focal deficits. Experimental end points were 48 hours (acute phase) and 7 days (subacute phase) of reperfusion. Sensorimotor assessment, elevated plus maze, and survival analysis were stroke outcome readouts. Brain samples were collected for quantitative real-time polymerase chain reaction, Western blot, and immunohistochemistry. In vitro ischemia in brain microvascular endothelial cells was used to investigate the direct effect of extracellular α-Syn.
resultsIn vivo, cerebral ischemia induced α-Syn 2.5-fold change gene expression, 2.7- to 3.2-fold-change protein oligomerization with apparent localization around cortical ischemic vessels. Improved subacute functional recovery linked to better survival was observed in C57BL/6S α-Syn null (87% to end point) versus C57BL/6J (45%) ischemic mice. The α-Syn null mice had reduced expression of
conclusionsThese findings indicate that ischemia-triggered pathological α-Syn leads to worse outcome in stroke mice by promoting endothelial inflammatory response and immune cell infiltration during the acute phase and by limiting angiogenesis in the subacute phase.
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.