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Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk
McQuade A, Blurton-Jones M.. Journal of molecular biology, 2019-02-07
Topic: Amyloid, tau and blood-test diagnosis
Research into the function of microglia has dramatically accelerated during the last few years, largely due to recent genetic findings implicating microglia in virtually every neurodegenerative disorder. In Alzheimer's disease (AD), a majority of risk loci discovered through genome-wide association studies were found in or near genes expressed most highly in microglia leading to the hypothesis that microglia play a much larger role in disease progression than previously thought. From this body of work produced in the last several years, we find that almost every function of microglia has been proposed to influence the progression of AD from altered phagocytosis and synaptic pruning to cytokine secretion and changes in trophic support.
Key findings
- In Alzheimer's disease (AD), a majority of risk loci discovered through genome-wide association studies were found in or near genes expressed most highly in microglia leading to the hypothesis that microglia play a much larger role in disease progression than previously thought.
- From this body of work produced in the last several years, we find that almost every function of microglia has been proposed to influence the progression of AD from altered phagocytosis and synaptic pruning to cytokine secretion and changes in trophic support.
- By studying key Alzheimer's risk genes such as TREM2, CD33, ABCA7, and MS4A6A, we will be able to distinguish true disease-modulatory pathways from the full range of microglial-related functions.
- To successfully carry out these experiments, more advanced microglial models are needed.
Why it matters
This review notes that most Alzheimer's disease risk loci found through genome-wide association studies lie in or near genes expressed most highly in microglia, and that nearly every microglial function has been proposed to influence disease progression. It does not report a treatment, cure or prevention for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 48/100
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 (Journal of molecular biology) |
| Journal's citation record | 3 / 4 | Journal of Molecular Biology: journal h-index 484 (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 | 2019 — 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 | 5 / 7 | Cited 241 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 26.8 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 4 / 6 | Cited 10.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 14 other studies in this library |
| Still being cited | 3 / 4 | Cited 82 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Mathew M. Blurton-Jones: h-index 57 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of California, Irvine: institution h-index 1,195 (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 30738892) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
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Read the original
- DOI: 10.1016/j.jmb.2019.01.045
- PubMed: 30738892
- Original source →
- Free full text: Journal of Molecular Biology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
McQuade, A., & Blurton-Jones, M. (2019). Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk. Journal of molecular biology. https://doi.org/10.1016/j.jmb.2019.01.045
Vancouver
McQuade A, Blurton-Jones M. Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk. Journal of molecular biology. 2019. doi:10.1016/j.jmb.2019.01.045. PMID: 30738892.
BibTeX
@article{mcquade2019-30738892,
author = {McQuade, A. and Blurton-Jones, M.},
title = {{Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk}},
journal = {Journal of molecular biology},
year = {2019},
doi = {10.1016/j.jmb.2019.01.045},
pmid = {30738892},
url = {https://doi.org/10.1016/j.jmb.2019.01.045}
}
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