Evidence mapPaperPMID 41157171Full record

ReviewLife (Basel, Switzerland)2025

Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.

Mario García-Domínguez

Abstract readReview
In one paragraph

Review in Life (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Mario García-DomínguezProgram of Immunology and Immunotherapy, CIMA-Universidad de Navarra, 31008 Pamplona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is accompanied by complex cellular and molecular changes that compromise CNS function. Among these, glial cells (astrocytes, microglia, and oligodendrocytes) play a central role in maintaining neural homeostasis, modulating synaptic activity, and supporting metabolic demands. Emerging evidence indicates that aging disrupts glial cell physiology through processes including mitochondrial dysfunction, impaired proteostasis, chronic low-grade inflammation, and altered intercellular signaling. These alterations contribute to synaptic decline, myelin degeneration, and persistent, low-grade inflammation of the CNS. This review synthesizes current knowledge on the bidirectional relationship between aging and glial cell dysfunction, highlighting how age-related systemic and CNS-specific factors exacerbate glial impairments and, in turn, accelerate neural deterioration. Finally, this study discusses some potential therapeutic strategies aimed at preserving or restoring glial function to promote CNS resilience in aging populations. Understanding this interplay offers critical opportunities for mitigating cognitive decline and improving quality of life in older adults.

Indexed as

agingastrocytesglial cellsinflammagingmicroglianeuroinflammationoligodendrocytessenescence

Identifiers

PMID41157171
PMCPMC12565160

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.