ReviewMedComm2025
Astrocyte in Neurological Disease: Pathogenesis and Therapy.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed.
- From neuroinflammation to immune reprogramming: Nanozyme-Integrated nanoplatforms for neuroimmune modulation in Parkinson's disease.Materials today. Bio · 2026Article
- Regenerative strategies for ALS: stem cells and extracellular vesicles.Discover nano · 2026Review
- Ficus virens in neurotherapeutics: bridging ethnomedicinal evidence with Nrf2/Keap1 and neuroinflammatory mechanisms.Molecular biology reports · 2026Review
- Curcumin in Alzheimer's Disease: From Mechanistic Insights to Translational Challenges and Emerging Curcuminoid Strategies.International journal of molecular sciences · 2026Review
- Astrocytic SCAP deletion ameliorates diabetes-associated cognitive impairment by suppressing microglial neuroinflammation and lipid droplet accumulation via the LCN2-24p3R-mTOR axis.Cell death & disease · 2026Article
- Astrocytic Redox Homeostasis as a Metabolic Modulator of DNA Damage and Repair in the Ischemic Penumbra.Cells · 2026Review
- Integrating weighted gene co-expression network analysis and machine learning reveal that NDUFA4L2 alleviates KA-induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction.Journal of bioenergetics and biomembranes · 2026Article
- Variants in glycine decarboxylase activate catabolic mechanisms of mitochondrial energy metabolism in the brain.The Journal of biological chemistry · 2026Article
- Beyond biochemical cascades: novel bio-mechanical and epigenetic paradigms of glial SASP in brain aging.Metabolic brain disease · 2026Review
- Supercritical CONutrients · 2026Article
- Lysophospholipids in Synucleinopathies: A Conceptual Framework Linking Proteostasis and Neuroinflammatory Signaling.Brain sciences · 2026Review
- Toxic Alpha-Synuclein and the Opening of the Gate: Blood-Brain Barrier Damage and Stepwise Leukocyte Infiltration.Cellular and molecular neurobiology · 2026Review
- Single-Cell Metabolic Profiling in a Glioblastoma Coculture Model Using AP-MALDI-Based Mass Spectrometry Imaging.Analytical chemistry · 2026Article
- Mitochondrial-Immune Dysfunction in MS: Therapeutic Potential of EV-Mediated Transfer.Cellular and molecular neurobiology · 2026Review
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination.Journal of neuroinflammation · 2026Article
- Review
- Sex Differences in Metabolite-Immune Circuits of Neuroinflammation.Immunological reviews · 2026Review
- CSF Leukocytes in Intracranial Infections: Diagnostic, Mechanistic, and Therapeutic Insights for Neurocritical Care.Cellular and molecular neurobiology · 2026Review
- Neuroinflammation at the Crossroads of Neurodegeneration: The Roles of Microglia and Astrocytes in Parkinson's Disease, Alzheimer's Disease, and Multiple Sclerosis.Neurosciences (Riyadh, Saudi Arabia) · 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
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes, as key support cells in the central nervous system, maintain homeostasis in the brain through mechanisms such as ionic homeostasis regulation, metabolic support, synaptic modulation, and neuroinflammatory regulation. Recent studies have shown that astrocyte dysfunction is closely related to the pathologic processes of various neurological diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and stroke. In this review, we comprehensively summarize the dual roles of astrocytes in neurological diseases: on one hand, their aberrant activation can exacerbate disease progression by mediating neuroinflammation, synaptic dysfunction, and blood-brain barrier disruption; on the other hand, their metabolic disorders, such as lipid droplet accumulation, mitochondrial dysfunction, and oxidative stress imbalance, further drive neurodegeneration. In terms of therapeutic strategies, interventions targeting astrocytes, such as modulation of activation phenotype, metabolic reprogramming, gene therapy, and innovative therapies based on exosomes and nanotechnology, show great promise. In the future, we may integrate multi-omics technologies and deepen clinical translational research to systematically analyze the spatial heterogeneity of astrocytes and their dynamic regulatory networks at different stages of the disease, in order to elucidate the precise mechanisms of their roles in the pathological process, and thus provide multidimensional theoretical support for the design of targeted therapeutic strategies.
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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.