ArticleNature neuroscience2026
A human-induced pluripotent stem cell-derived spheroid model to investigate myelin injury and repair.
Article in Nature neuroscience, 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
22 authors.
Funding
Abstract
There are no currently approved therapies that promote new myelin formation after myelin damage, which can, in part, be attributed to a lack of reliable systems that can reproducibly model these processes. Here we engineered a human iPSC-derived spheroid model enriched with mature, myelinating oligodendrocytes and functionally reactive microglia. This model enables the study of human central nervous system remyelination after a demyelinating insult by recapitulating processes of myelin damage and repair. These include myelin fragmentation, microglial reactivity and phagocytosis of myelin debris, oligodendrocyte generation and differentiation, and axonal ensheathment with newly formed myelin. We show that newly generated oligodendrocytes contribute to remyelination, and use ultrastructural quantification to demonstrate that remyelinated axons are ensheathed by thinner myelin after injury. Altogether, we provide a model to interrogate otherwise inaccessible aspects of human myelin biology relevant to multiple sclerosis, providing mechanistic insights into disease pathways and a platform for drug screening.
Identifiers
42823475What 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.