ReviewGlia2025
Oligodendrogenesis in Evolution, Development and Adulthood.
Review in Glia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease.Neuroscience bulletin · 2026Review
- Cerebellar oligodendrocytic α-synuclein pathology and dentate nucleus neuronal hypertrophy in Parkinson's disease.Scientific reports · 2026Article
- Evolutionarily informed gene sets reveal conserved and lineage-modified transcriptional programs during vertebrate forebrain evolution.bioRxiv : the preprint server for biology · 2026Article
- Klotho Function in Neurogenesis and Oligodendrogenesis: A Mini-Review Update.Journal of molecular neuroscience : MN · 2026Review
- Light-based 40 Hz sensory therapy for brain disorders: physiological basis, therapeutic mechanisms, and future prospects.Frontiers in medicine · 2026Review
- Specific genetic and biological patterns underlying cortical morphological alterations in vascular cognitive impairment.Alzheimer's research & therapy · 2025Article
- Oligodendrocyte lineage cells dysfunction in depression: early life stress, adolescent vulnerability and the emerging role of lipid metabolism.Translational psychiatry · 2025Review
- Novel Animal Models for Multiple Sclerosis: R-Ras GTPases in Myelin Pathophysiology.Biomolecules · 2025Review
- Review
- Glial Diversity and Evolution: Insights from Teleost Fish.Brain sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Oligodendrogenesis and myelin formation are important processes in the central nervous system (CNS) of jawed vertebrates, underpinning the highly efficient neural computation within the compact CNS architecture. Myelin, the dense lipid sheath wrapped around axons, enables rapid signal transmission and modulation of neural circuits. Oligodendrocytes are generated from oligodendrocyte precursor cells (OPCs), which are widely distributed in the adult CNS and continue to produce new oligodendrocytes throughout life. Adult oligodendrogenesis is integral to adaptive myelination, which fine-tunes neural circuits in response to neuronal activity, contributing to neuroplasticity, learning, and memory. Emerging evidence also highlights the role of oligodendrogenesis in specialized brain regions, linking oligodendrocytes to metabolic and homeostatic functions. In the aging and diseased brain, dysregulated oligodendrogenesis exacerbates myelin loss and may contribute to pathogenesis. In addition, maladaptive myelination driven by aberrant neuronal activity could sustain a dysfunction in conditions such as epilepsy. This review summarizes the current understanding of oligodendrogenesis, with insights into its evolution, regulation, and impact on aging and disease.
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.