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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer's disease (AD). Human genetics data point to a key role for microglia in the pathogenesis of AD. The majority of risk genes for AD are highly expressed (and many are selectively expressed) by microglia in the brain. There is mounting evidence that microglia protect against the incidence of AD, as impaired microglial activities and altered microglial responses to β-amyloid are associated with increased AD risk. On the other hand, there is also abundant evidence that activated microglia can be harmful to neurons. Microglia can mediate synapse loss by engulfment of synapses, likely via a complement-dependent mechanism; they can also exacerbate tau pathology and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic astrocytes. Gene expression profiles indicate multiple states of microglial activation in neurodegenerative disease settings, which might explain the disparate roles of microglia in the development and progression of AD pathology.

Why it matters

Summarizes evidence on microglia in Alzheimer's disease. Most Alzheimer's risk genes are highly expressed by microglia, and there is evidence both that microglia protect against the disease and that activated microglia can harm neurons, for example by engulfing synapses and worsening tau pathology.

How this study scored 56/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence left out, no data; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 7 of 7; Citations per year 5 of 5; Impact for its field and year 5 of 6; Cited by studies here 0 of 6; Still being cited 4 of 4; Senior author's track record 4 of 4; Institution's track record 1 of 3; Multi-centre collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. 53 of the 95 points it could be judged on, which is 56 of 100. Total 56 of 100.53 of the 95 points we could judge = 56 of 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. We have no data on strength of evidence, so that was left out: it earned 53 of the 95 points we could judge it on, which is 56 out of 100.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (The Journal of Cell Biology)
Journal's citation record 4 / 4 The Journal of Cell Biology: journal h-index 597 (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 — / 5 No evidence rating recorded — left out of this score
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 2 / 5 2017 — 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 7 / 7 Cited 1,928 times (OpenAlex, 2026-10-10)
Citations per year 5 / 5 175.3 citations a year over 11 year(s) since 2017
Impact for its field and year 5 / 6 Cited 35.3× 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 4 / 4 Cited 789 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 0 countries — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 29196460)
Free to read 2 / 2 Free to read
Points 53 / 95 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 53 of the 95 points we could judge it on is 56 out of 100.
Total 56 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

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

Hansen, D. V., Hanson, J. E., & Sheng, M. (2017). Microglia in Alzheimer’s disease. The Journal of Cell Biology. https://doi.org/10.1083/jcb.201709069

Vancouver

Hansen DV, Hanson JE, Sheng M. Microglia in Alzheimer’s disease. The Journal of Cell Biology. 2017. doi:10.1083/jcb.201709069. PMID: 29196460.

BibTeX

@article{hansen2017-29196460,
  author  = {Hansen, David V. and Hanson, Jesse E. and Sheng, Morgan},
  title   = {{Microglia in Alzheimer’s disease}},
  journal = {The Journal of Cell Biology},
  year    = {2017},
  doi     = {10.1083/jcb.201709069},
  pmid    = {29196460},
  url     = {https://doi.org/10.1083/jcb.201709069}
}

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