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58/100

✓ Peer-reviewed alzhub usefulness score 58 out of 100. TREM2 and immune genetics

Topic: Brain proteins, microglia and lab models

The role of microglia in the amyloid cascade of Alzheimer's disease (AD) is debated due to conflicting findings. Using a genetic and a pharmacological approach we demonstrate that depletion of microglia before amyloid-β (Aβ) plaque deposition, leads to a reduction in plaque numbers and neuritic dystrophy, confirming their role in plaque initiation. Transplanting human microglia restores Aβ plaque formation.

Key findings

Using a genetic and a pharmacological approach we demonstrate that depletion of microglia before amyloid-β (Aβ) plaque deposition, leads to a reduction in plaque numbers and neuritic dystrophy, confirming their role in plaque initiation.
Transplanting human microglia restores Aβ plaque formation.
While microglia depletion reduces insoluble Aβ levels, soluble Aβ concentrations stay consistent, challenging the view that microglia clear Aβ.
In later stages, microglial depletion decreases plaque compaction and increases neuritic dystrophy, suggesting a protective role.

Why it matters

Using genetic and pharmacological approaches, this study found that depleting microglia before amyloid-β plaque deposition reduced plaque numbers and neuritic dystrophy, while transplanting human microglia restored plaque formation. It also found that microglia depletion reduces insoluble but not soluble amyloid-β, challenging the view that microglia clear amyloid-β, and it is animal work rather than a treatment.

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Study details

Evidence strengthLow

How this study scored 58/100

Published in a leading specialty 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	9 / 10	Tier 2 — leading specialty journal (Nature communications)
Journal's citation record	4 / 4	Nature Communications: journal h-index 747 (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	4 / 5	2024 — within 3 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 115 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	28.8 citations a year over 4 year(s) since 2024
Impact for its field and year	4 / 6	Cited 15.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 5 other studies in this library
Still being cited	3 / 4	Cited 115 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Bart De Strooper: h-index 146 (OpenAlex, whole career)
Institution's track record	2 / 3	University College London: institution h-index 2,029 (OpenAlex)
Multi-centre collaboration	2 / 3	OpenAlex lists 8 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 39639016)
Free to read	2 / 2	Free to read
Total	58 / 100	—

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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. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

APA 7th

Baligács, N., Albertini, G., Borrie, S. C., Serneels, L., Pridans, C., Balusu, S., et al. (2024). Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer's Disease. Nature communications. https://doi.org/10.1038/s41467-024-54779-w

Vancouver

Baligács N, Albertini G, Borrie SC, Serneels L, Pridans C, Balusu S, et al. Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer's Disease. Nature communications. 2024. doi:10.1038/s41467-024-54779-w. PMID: 39639016.

BibTeX

@article{baligacs2024-39639016,
  author  = {Baligács, N. and Albertini, G. and Borrie, S. C. and Serneels, L. and Pridans, C. and Balusu, S. and De Strooper, B.},
  title   = {{Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer's Disease}},
  journal = {Nature communications},
  year    = {2024},
  doi     = {10.1038/s41467-024-54779-w},
  pmid    = {39639016},
  url     = {https://doi.org/10.1038/s41467-024-54779-w}
}

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