ReviewExperimental neurology2026
White matter injury after brain ischemia.
Review in Experimental neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Emodin Suppresses the RAGE/ROCK1 Pathway to Modulate the Oligodendrocyte Lineage and Ameliorate Demyelination in Vascular Dementia Rats.CNS neuroscience & therapeutics · 2026Article
- Novel Benzofuran Derivatives as SARM1 Inhibitors for Treating Axonal Degeneration.ACS medicinal chemistry letters · 2026Article
- Novel Pyrrolidinone Derivatives as SARM1 Inhibitors for Treating Axonal Degeneration.ACS medicinal chemistry letters · 2026Article
- Post-ischemic modification of neurogenesis and oligodendrogenesis in rodent models.Frontiers in neural circuits · 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
5 authors.
Funding
Abstract
Ischemic white matter injury (WMI) is a significant concern in various clinical settings, particularly affecting the elderly and those with comorbidities such as hypoxia and hyperglycemia. Ischemic WMI can be caused either by primary WM ischemia, or secondary axonal injury as a result of the loss of the "remote" axonal parent neurons or the depletion of adhesive and neurotrophic molecules following post-synaptic neuronal death in the grey matter after focal ischemia. While neurons are highly vulnerable to ischemia, potentially undergoing cell death after an ischemic duration longer than a just few minutes, oligodendrocyte (OLG) lineage cells and axons show somewhat greater initial resistant to ischemia but ultimately suffer various degrees of damage after prolonged ischemia exposure. WMI typically progresses over time from initial demyelination to OLG death and axonal injury, followed by varying degrees of OLG biogenesis, remyelination, axonal sprouting, and synaptic reconnections. The severity of ischemic WMI is a key predictor of poor long-term outcome in brain ischemia-related conditions. Despite its clinical importance, ischemic WMI remains significantly understudied in preclinical animal models, creating a weak link in the field of ischemic brain injury animal research. Many molecular and pathological mechanisms underlying post-ischemic WMI remain poorly understood, and currently, no specific treatments exist for WMI patients. This review aims to stimulate WMI research by providing updated knowledge, emerging hypotheses, and future research directions to foster understanding the mechanisms and to guide the development of the effective therapeutic strategies.
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.