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Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies
Flávia Carvalho Alcântara Gomes, Isadora C. Pereira Matias. Journal of Neurochemistry, 2026-05-01
Topic: Brain proteins, microglia and lab models
The increase in senescent cells, including glial cells in the brain, is a general feature of normal aging and has been associated with age-related pathologies. Although recent evidence suggests that astrocytes undergo senescence in these conditions, little is known about the molecular, and cellular mechanisms underlying this event. We discuss how astrocyte aging contributes to cognitive decline and highlight emerging evidence on how targeting astrocytes, both genetically and pharmacologically, may rescue cognitive decline associated with aging and neurodegenerative diseases. In this context, recent studies indicate that astrocytes undergo significant molecular and functional remodeling during aging. Notably, astrocyte senescence has been associated with loss of lamin-B1, nuclear alterations, impaired synaptogenic and neuritogenic capacity, altered glutamate metabolism, and mitochondrial dysfunction, all of which may contribute to reduced neuronal support and circuit integrity. In parallel, recent advances have shown that astrocyte responses during aging also include diverse reactive states that vary according to brain region, microenvironment, and disease stage. Together, current evidence indicates that astrocyte dysfunction in aging reflects a complex and dynamic spectrum of cellular states that play a central role in brain vulnerability and represent promising targets for intervention in aging and neurodegenerative diseases.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gomes, F. C. A., & Matias, I. C. P. (2026). Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies. Journal of Neurochemistry. https://doi.org/10.1111/jnc.70459
Vancouver
Gomes FCA, Matias ICP. Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies. Journal of Neurochemistry. 2026. doi:10.1111/jnc.70459. PMID: 42138465.
BibTeX
@article{gomes2026-42138465,
author = {Gomes, Flávia Carvalho Alcântara and Matias, Isadora C. Pereira},
title = {{Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies}},
journal = {Journal of Neurochemistry},
year = {2026},
doi = {10.1111/jnc.70459},
pmid = {42138465},
url = {https://doi.org/10.1111/jnc.70459}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- The increase in senescent cells, including glial cells in the brain, is a general feature of normal aging and has been associated with age-related pathologies.
- Although recent evidence suggests that astrocytes undergo senescence in these conditions, little is known about the molecular, and cellular mechanisms underlying this event.
- We discuss how astrocyte aging contributes to cognitive decline and highlight emerging evidence on how targeting astrocytes, both genetically and pharmacologically, may rescue cognitive decline associated with aging and neurodegenerative diseases.
- In this context, recent studies indicate that astrocytes undergo significant molecular and functional remodeling during aging.
- Notably, astrocyte senescence has been associated with loss of lamin-B1, nuclear alterations, impaired synaptogenic and neuritogenic capacity, altered glutamate metabolism, and mitochondrial dysfunction, all of which may contribute to reduced neuronal support and circuit integrity.
Why it matters
This review discusses how aging astrocytes contribute to cognitive decline and notes that targeting astrocytes genetically or pharmacologically may rescue decline in aging and neurodegenerative disease. It is a discussion of emerging evidence, not a proven treatment.
Study details
- Evidence strengthLow
How this study scored 37/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Neurochemistry) |
| Journal's citation record | 3 / 4 | Journal of Neurochemistry: journal h-index 349 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 3 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.5 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 3 / 6 | Cited 7.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Isadora C. Pereira Matias: h-index 15 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Universidade Federal do Rio de Janeiro: institution h-index 617 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 42138465) |
| Free to read | 2 / 2 | Free to read |
| Total | 37 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/jnc.70459
- PubMed: 42138465
- Original source →
- Free full text: Journal of Neurochemistry →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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