Microglia in Brain Development, Homeostasis, and Neurodegeneration
Bohlen CJ, Friedman BA, Dejanovic B, Sheng M.. Annual review of genetics, 2019-09-13
Topic: Brain proteins, microglia and lab models
Advances in human genetics have implicated a growing number of genes in neurodegenerative diseases, providing insight into pathological processes. For Alzheimer disease in particular, genome-wide association studies and gene expression studies have emphasized the pathogenic contributions from microglial cells and motivated studies of microglial function/dysfunction. Here, we summarize recent genetic evidence for microglial involvement in neurodegenerative disease with a focus on Alzheimer disease, for which the evidence is most compelling. To provide context for these genetic discoveries, we discuss how microglia influence brain development and homeostasis, how microglial characteristics change in disease, and which microglial activities likely influence the course of neurodegeneration. In all, we aim to synthesize varied aspects of microglial biology and highlight microglia as possible targets for therapeutic interventions in neurodegenerative disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Bohlen, C. J., Friedman, B. A., Dejanovic, B., & Sheng, M. (2019). Microglia in Brain Development, Homeostasis, and Neurodegeneration. Annual review of genetics. https://doi.org/10.1146/annurev-genet-112618-043515
Vancouver
Bohlen CJ, Friedman BA, Dejanovic B, Sheng M. Microglia in Brain Development, Homeostasis, and Neurodegeneration. Annual review of genetics. 2019. doi:10.1146/annurev-genet-112618-043515. PMID: 31518519.
BibTeX
@article{bohlen2019-31518519,
author = {Bohlen, C. J. and Friedman, B. A. and Dejanovic, B. and Sheng, M.},
title = {{Microglia in Brain Development, Homeostasis, and Neurodegeneration}},
journal = {Annual review of genetics},
year = {2019},
doi = {10.1146/annurev-genet-112618-043515},
pmid = {31518519},
url = {https://doi.org/10.1146/annurev-genet-112618-043515}
}
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
- Advances in human genetics have implicated a growing number of genes in neurodegenerative diseases, providing insight into pathological processes.
- For Alzheimer disease in particular, genome-wide association studies and gene expression studies have emphasized the pathogenic contributions from microglial cells and motivated studies of microglial function/dysfunction.
- Here, we summarize recent genetic evidence for microglial involvement in neurodegenerative disease with a focus on Alzheimer disease, for which the evidence is most compelling.
- To provide context for these genetic discoveries, we discuss how microglia influence brain development and homeostasis, how microglial characteristics change in disease, and which microglial activities likely influence the course of neurodegeneration.
- In all, we aim to synthesize varied aspects of microglial biology and highlight microglia as possible targets for therapeutic interventions in neurodegenerative disease.
Why it matters
This review summarizes genetic evidence that microglial cells contribute to Alzheimer's disease and other neurodegenerative conditions. It highlights microglia as possible targets for future therapies, but it is a summary of research and not a treatment or cure.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 46/100
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 (Annual review of genetics) |
| Journal's citation record | 3 / 4 | Annual Review of Genetics: journal h-index 297 (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 212 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 23.6 citations a year over 9 year(s) since 2019 |
| 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 | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 99 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Morgan Sheng: h-index 142 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Genentech: institution h-index 1,144 (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 31518519) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1146/annurev-genet-112618-043515
- PubMed: 31518519
- Original source →
- Free full text: annualreviews.org →
Full text: free to read — Unpaywall lists this copy as free to read: the link above (checked 10 Oct 2026).
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