Evidence map›Paper›PMID 42321809›Full record

ArticleCell communication and signaling : CCS2026

Bacteria-derived glutarate mitigates Alzheimer's disease model pathology through autophagy-lysosomal pathway.

Cui Deng, Mingqin Qu, Wei Yao, Xiaotong Hu, Yan Li, Weilun Zheng, Yiying Zhai, Fangyan Liu, Ting Yang, Tianlong Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Cui Deng *Department of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Mingqin Qu *Department of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Wei Yao *Department of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Xiaotong HuDepartment of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Yan LiDepartment of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Weilun ZhengDepartment of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Yiying ZhaiDepartment of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Fangyan LiuDepartment of Anesthesiology, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing, 100053, China.
Ting YangDepartment of Anesthesiology, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing, 100053, China.
Tianlong WangDepartment of Anesthesiology, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing, 100053, China.
Xiangming WangDepartment of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing, 100069, China. xm224@sohu.com.

Funding

National Natural Science Foundation of China 32571125
6 · The paper itself

Abstract

Probiotics exert neuroprotective effects against Alzheimer's disease (AD) by modulating gut-brain axis pathways, though disease-modifying therapies remain unavailable. Our study revealed that Escherichia coli (E. coli) strain HB101 ameliorated AD-related phenotypes in Caenorhabditis elegans‌ (C. elegans) models, including learning deficits, neurodegeneration, and paralysis. Mechanistically, HB101 reduced amyloid-β (Aβ) aggregation by enhancing lysosomal activity, autophagy, and mitochondrial/endoplasmic reticulum unfolded protein responses (UPRmt/UPRer). Specifically, HB101 activated UPRmt via atfs-1 and sphk-1, and UPRer through pek-1. Metabolomic screening pinpointed glutarate as a bioactive metabolite that mitigates AD-related pathology through lysosomal activation and autophagy promotion.

Indexed as

Alzheimer DiseaseAutophagyEscherichia coliGlutaratesLysosomesAmyloid beta-PeptidesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDisease Models, AnimalSignal TransductionUnfolded Protein ResponseAmyloid beta-PeptidesCaenorhabditis elegans ProteinsGlutaratesAlzheimer’s diseaseAutophagyC. elegansLysosomeProbiotics

Identifiers

PMID42321809
PMCPMC13531758

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.