ArticleStroke2026
Juvenile Mice Develop Infarct-Induced Neurodegeneration and Emerging Cognitive Decline in a Model of Pediatric Stroke.
Article in Stroke, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundOver half of pediatric stroke survivors have permanent cognitive deficits, which can emerge late after stroke. Mechanisms of cognitive decline after pediatric stroke may differ from those in adults because children's strokes occur while brain and immune development are still ongoing. We therefore aimed to develop a pediatric mouse model of infarct-induced delayed cognitive decline to define age-related differences in immune responses compared with adults.
methodsMale and female C57BL/6J mice were randomized to stroke or sham surgery at 28 days old to model stroke in late childhood. We used permanent distal middle cerebral artery occlusion followed by 60 minutes of hypoxia to induce an ischemic cortical stroke. Juvenile mice underwent behavioral testing at 1 and 7 weeks after surgery using Barnes maze and Novel Object Recognition tests. We quantified stroke size, atrophy, and neuroinflammation at 3 days and 7 weeks after surgery in juvenile and adult mice using immunostaining.
resultsOne week after surgery, juvenile stroke and sham mice performed comparably on cognitive testing. However, by 7 weeks after surgery, stroke mice of both sexes performed significantly worse on reversal learning with the Barnes maze. Histologically, juvenile mice had greater innate immune activation at sites of secondary neurodegeneration in the corpus callosum, corticospinal tract, and thalamus at 3 days after stroke, while adults had greater chronic innate immune activity at these sites 7 weeks after stroke.
conclusionsIn a model of childhood ischemic stroke, juvenile mice of both sexes developed an emerging cognitive deficit analogous to that seen in pediatric stroke survivors. It was associated with chronic neuroinflammation in uninjured subcortical structures that undergo secondary neurodegeneration. Our results suggest that infarct-induced neurodegeneration occurs after stroke in juvenile mice, and that there are age-related divergent trajectories in the innate immune response to stroke at sites of secondary neurodegeneration.
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.