ReviewIBRO neuroscience reports2026
Secondary demyelination after stroke: Glial cell crosstalk.
Review in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroglial cells serve as the myelinating cells in the central nervous system and are essential for axonal integrity and function. Following a stroke, progressive loss of myelin occurs in white matter regions distal to the infarct core, contributing to cognitive decline and even dementia. Recent research has revealed that the central mechanism involves a cascading response triggered by disruption of the astrocyte-microglia-oligodendrocyte axis. Astrocyte-secreted lipocalin-2 acts as a key driver of myelin degradation and axonal energy crisis by inducing iron influx, triggering oxidative stress, and causing mitochondrial dysfunction. An imbalance in microglial subpopulations, along with oligodendrocyte apoptosis, further exacerbates demyelination. Although no therapies are currently approved, novel strategies targeting lipocalin-2 blockade, mitochondrial repair, and immune modulation offer new hope for preserving white matter function.
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