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30/100

✓ Peer-reviewed alzhub usefulness score 30 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

Objective To explore the intrinsic relationship between microglia in Alzheimer′s disease (AD) and natural aging, and their role in mediating microenvironmental proteostasis. Methods Nearly 1.69 million brain single-cell and single-nucleus transcriptomes from 18 public datasets were integrated and annotated using deep generative models. A “transcriptomic aging score” was constructed to compare the transcriptional remodeling of microglia between natural aging and AD models. Multiplex immunofluorescence staining on brain sections was performed to verify the in situ expression of key molecules for proteostasis and lysosomes. A Trem2-deficient model was introduced to explore the regulatory mechanisms. Results AD pathology significantly accelerated the age-dependent accumulation of late-stage disease-associated microglia (DAM-Late). The AD transcriptional profile showed a highly significant positive correlation with natural aging (R=0.481), manifesting as a “pathological amplification” of aging-mediated lipid metabolism and lysosomal programs. Metabolic stress led to the collapse of microglial proteostasis, with a significant increase in the area and number of αB-CRYSTALLIN, CD68, and UBC puncta carried by single cells in the hypothalamus of AD mice. TREM2 acted as a key switch initiating the compensatory program, and its deficiency led to phenotypic decoupling and functional compensation failure. Conclusions The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. Under continuous pathological stress, this adaptive compensation may ultimately mediate severe impairment of proteostasis in the microenvironment and adjacent cells.

Key findings

Results AD pathology significantly accelerated the age-dependent accumulation of late-stage disease-associated microglia (DAM-Late).
The AD transcriptional profile showed a highly significant positive correlation with natural aging (R=0.481), manifesting as a “pathological amplification” of aging-mediated lipid metabolism and lysosomal programs.
Metabolic stress led to the collapse of microglial proteostasis, with a significant increase in the area and number of αB-CRYSTALLIN, CD68, and UBC puncta carried by single cells in the hypothalamus of AD mice.
Conclusions The pathological activation of AD microglia significantly amplifies endogenous aging characteristics.

Why it matters

In mice, Alzheimer's pathology accelerated the accumulation of late-stage disease-associated microglia and amplified aging-related lipid and lysosomal programs, with a collapse of microglial proteostasis. TREM2 acted as a key switch for this compensatory program, suggesting a possible target, but this is animal and cell-based work only.

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Study details

Evidence strengthLow

How this study scored 30/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record and senior author's track record, so those were left out: it earned 28 of the 92 points we could judge it on, which is 30 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (DOAJ (DOAJ: Directory of Open Access Journals))
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
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	5 / 5	2026 — within 1 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	Laboratory or animal study (title names “mice”) — scores zero
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 2 year(s) since 2026
Impact for its field and year	0 / 6	Cited 0.0× 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	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	OpenAlex's profile for last-listed author LI Bingnan ZHOU Ziqun holds only 1 work(s), too few to judge a track record — left out of this score
Institution's track record	1 / 3	Chinese Academy of Medical Sciences & Peking Union Medical College: institution h-index 950 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	1 / 2	Not in PubMed, but has a DOI
Free to read	2 / 2	Free to read
Points	28 / 92	Scored on 18 of 20 parts. We have no data for the rest, so they are left out: 28 of the 92 points we could judge it on is 30 out of 100.
Total	30 / 100	—

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Read the original

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Cite this study APA, Vancouver, BibTeX · download .bib or .ris

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APA 7th

Ziqun, L. I. B. Z. H. O. U. (2026). Single-cell atlas reveals pathological amplification of aging programs and proteostasis collapse in microglia of Alzheimer′s disease mice. DOAJ (DOAJ: Directory of Open Access Journals). https://doi.org/10.16352/j.issn.1001-6325.2026.06.0791

Vancouver

Ziqun LIBZHOU. Single-cell atlas reveals pathological amplification of aging programs and proteostasis collapse in microglia of Alzheimer′s disease mice. DOAJ (DOAJ: Directory of Open Access Journals). 2026. doi:10.16352/j.issn.1001-6325.2026.06.0791.

BibTeX

@article{ziqun2026-46a316ba,
  author  = {Ziqun, LI Bingnan ZHOU},
  title   = {{Single-cell atlas reveals pathological amplification of aging programs and proteostasis collapse in microglia of Alzheimer′s disease mice}},
  journal = {DOAJ (DOAJ: Directory of Open Access Journals)},
  year    = {2026},
  doi     = {10.16352/j.issn.1001-6325.2026.06.0791},
  url     = {https://doi.org/10.16352/j.issn.1001-6325.2026.06.0791}
}

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