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Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease
Villegas-Llerena C, Phillips A, Garcia-Reitboeck P, Hardy J, Pocock JM.. Current opinion in neurobiology, 2015-10-24
Topic: Brain proteins, microglia and lab models
Neuroinflammation is a pathological hallmark of Alzheimer's disease (AD), and microglia, the brain's resident phagocyte, are pivotal for the immune response observed in AD. Microglia act as sentinel and protective cells, but may become inappropriately reactive in AD to drive neuropathology. Recent Genome Wide Association Studies (GWAS) have identified more than 20 gene variants associated with an increased risk of late-onset AD (LOAD), the most prevalent form of AD [1].
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Villegas-Llerena, C., Phillips, A., Garcia-Reitboeck, P., Hardy, J., & Pocock, J. M. (2016). Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease. Current opinion in neurobiology. https://doi.org/10.1016/j.conb.2015.10.004
Vancouver
Villegas-Llerena C, Phillips A, Garcia-Reitboeck P, Hardy J, Pocock JM. Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease. Current opinion in neurobiology. 2016. doi:10.1016/j.conb.2015.10.004. PMID: 26517285.
BibTeX
@article{villegasllerena2016-26517285,
author = {Villegas-Llerena, C. and Phillips, A. and Garcia-Reitboeck, P. and Hardy, J. and Pocock, J. M.},
title = {{Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease}},
journal = {Current opinion in neurobiology},
year = {2016},
doi = {10.1016/j.conb.2015.10.004},
pmid = {26517285},
url = {https://doi.org/10.1016/j.conb.2015.10.004}
}
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Key findings
- Microglia act as sentinel and protective cells, but may become inappropriately reactive in AD to drive neuropathology.
- Recent Genome Wide Association Studies (GWAS) have identified more than 20 gene variants associated with an increased risk of late-onset AD (LOAD), the most prevalent form of AD [1].
- The findings strongly implicate genes related to the immune response (CR1, CD33, MS4A, CLU, ABCA7, EPHA1 and HLA-DRB5-HLA-DRB1), endocytosis (BIN1, PICALM, CD2AP, EPHA1 and SORL1) and lipid biology (CLU, ABCA7 and SORL1) [2-8], and many encode proteins which are highly expressed in microglia [1].
- Furthermore, recent identification of a low frequency mutation in the gene encoding the triggering receptor expressed in myeloid cells 2 protein (TREM2) confers increased risk of AD in LOAD cohorts with an effect size similar to that for APOE, until recently the only identified genetic risk factor associated with LOAD [9,10(••)] (Figure 1).
Why it matters
This review describes how microglia can be protective but may become inappropriately reactive and drive neuropathology in Alzheimer's disease. It reports that many gene variants linked to late-onset Alzheimer's relate to the immune response, endocytosis and lipid biology, but offers no treatment.
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 (Current opinion in neurobiology) |
| Journal's citation record | 3 / 4 | Current Opinion in Neurobiology: journal h-index 306 (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 | 1 / 5 | 2016 — within 20 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 270 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.5 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 2 / 6 | Cited 2.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 25 other studies in this library |
| Still being cited | 3 / 4 | Cited 57 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jennifer M. Pocock: h-index 44 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26517285) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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