ArticleCNS neuroscience & therapeutics2025
Single-Cell RNA Sequencing and Spatial Transcriptomics Reveal a Novel Mechanism of Oligodendrocyte-Neuron Interaction in Cognitive Decline After High-Altitude Cerebral Edema.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed.
- Chronic high-altitude exposure and intracerebral hemorrhage: A novel perspective from the vascular-immune-neuronal network.Neuroprotection (Chichester, England) · 2026Review
- RPS29 as a potential early diagnostic biomarker for necrotizing enterocolitis: validation from transcriptomic and proteomic cohorts.Translational pediatrics · 2026Article
- High-altitude hypoxia drives dentate gyrus neuronal vulnerability through an IL1α-astrocyte-SLC1A2 pathway.Journal of neuroinflammation · 2026Article
- Breast cancer stem cell activity driven byWorld journal of stem cells · 2026Article
- High-altitude hypoxic cues and cerebral ischemic tolerance: an evidence-graded translational framework for stroke research.Frontiers in neuroscience · 2026Review
- The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026Review
- Single-Cell RNA Sequencing and Spatial Transcriptomics Reveal a Novel Mechanism of Oligodendrocyte-Neuron Interaction in Cognitive Decline After High-Altitude Cerebral Edema.CNS neuroscience & therapeutics · 2025Article
- Unraveling the complexity of cognitive impairment following high-altitude exposure: from preclinical animal models to human organoids.Frontiers in neuroscience · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
backgroundHigh-altitude cerebral edema (HACE) leads to cognitive decline, but the underlying cellular and molecular mechanisms remain unclear.
methodsWe established a mouse model of HACE under hypobaric hypoxia (simulating at an altitude of 6000 m) and analyzed hippocampal changes using single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) at 3 days and 7 days post-exposure.
resultsHypobaric hypoxia induced HACE and cognitive decline by altering the transcriptomic profiles and interactions of oligodendrocytes (MOL and MOL2) and neurons (ExN-L6-CT-2). Early upregulation of PI3K/mTOR in oligodendrocytes mitigated Rps29-bax-mediated ribosomal stress and oxidative phosphorylation, promoting survival and myelin repair. Prolonged hypoxia suppressed PI3K/mTOR, triggering apoptosis/autophagy via oxidative phosphorylation and ribosomal stress. Enhanced Tnfrsf21-App interactions between MOL2 and ExN-L6-CT-2 exacerbated neuroinflammation and cognitive decline.
conclusionsOur study reveals that HACE-induced cognitive impairment is closely associated with dysregulated ribosomal stress and oxidative phosphorylation and impaired neuroactive ligand-receptor interactions. Furthermore, we identify PI3K/mTOR dynamics, Rps29-bax-axis, and Tnfrsf21-App as novel regulators, offering potential therapeutic targets.
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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.