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Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration
Afridi R, Lee WH, Suk K.. Frontiers in cellular neuroscience, 2020-08-13
Topic: Brain proteins, microglia and lab models
Age-related chronic inflammatory activation of microglia and their dysfunction are observed in many neurodegenerative diseases, and the potential contributions of these dysfunctional cells to neurodegeneration have been demonstrated recently. The housekeeping and defensive functions of microglia, such as surveying the brain parenchyma and phagocytosis of neuronal debris after injury, are important for brain homeostasis and immunity. During neurodegenerative diseases, loss of these functions can promote disease pathology by producing proinflammatory cytokines and increasing oxidative stress, which can exaggerate the ongoing neuroinflammation.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Afridi, R., Lee, W. H., & Suk, K. (2020). Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration. Frontiers in cellular neuroscience. https://doi.org/10.3389/fncel.2020.00246
Vancouver
Afridi R, Lee WH, Suk K. Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration. Frontiers in cellular neuroscience. 2020. doi:10.3389/fncel.2020.00246. PMID: 32903682.
BibTeX
@article{afridi2020-32903682,
author = {Afridi, R. and Lee, W. H. and Suk, K.},
title = {{Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration}},
journal = {Frontiers in cellular neuroscience},
year = {2020},
doi = {10.3389/fncel.2020.00246},
pmid = {32903682},
url = {https://doi.org/10.3389/fncel.2020.00246}
}
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 housekeeping and defensive functions of microglia, such as surveying the brain parenchyma and phagocytosis of neuronal debris after injury, are important for brain homeostasis and immunity.
- During neurodegenerative diseases, loss of these functions can promote disease pathology by producing proinflammatory cytokines and increasing oxidative stress, which can exaggerate the ongoing neuroinflammation.
- A recent surge in microglial research has unraveled myriads of microglial phenotypes associated with aging and neurodegenerative diseases, in addition to the conventional M1/M2 paradigm.
- Each of these phenotypes can be characterized by distinct transcriptional profiles as well as altered metabolism, migration, and phagocytosis characteristics.
Why it matters
This review describes how loss of normal microglial functions during neurodegenerative diseases can promote pathology by producing proinflammatory cytokines and increasing oxidative stress. It discusses mechanisms but does not test a treatment or cure.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in cellular neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Cellular Neuroscience: journal h-index 175 (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 | 2 / 5 | 2020 — within 10 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 65 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.1 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 2 / 6 | Cited 2.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 32 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Kyoungho Suk: h-index 69 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Kyungpook National University: institution h-index 518 (OpenAlex) |
| Multi-centre 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 32903682) |
| Free to read | 2 / 2 | Free to read |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fncel.2020.00246
- PubMed: 32903682
- Original source →
- Free full text: Frontiers in Cellular Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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