Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.
Overview
- Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, The Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan 523808, China
- Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China
- Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China
Abstract
Andrographolide (AP), a diterpenoid extracted from Andrographis paniculata, has emerged as a promising treatment for Alzheimer’s disease (AD) in preclinical studies, but the underlying mechanisms remain incompletely defined. Here, we demonstrated that AP treatment improved cognition performance and reduced amyloid-β (Aβ) plaque accumulation in 5×FAD transgenic mice of both sexes, by mitigating microglial senescence. Proteomic analysis revealed that AP markedly decreased cholesterol content in the cerebral cortex. Using an in vitro low-density lipoprotein-induced senescence model, we found that AP significantly alleviated senescence in BV2 microglia while enhancing their phagocytic capacity. Mechanistically, AP mitigated microglial senescence by inhibiting STAT3 signaling. Overall, these findings identify a previously unrecognized immunometabolic mechanism for AP in the treatment of AD.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
The paper's code and data availability statement is in the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data and code availability
All datasets used in this study are available from the corresponding author upon reasonable request. The mass data used in this study have been deposited in the ProteomeXchange Consortium with the iProX partner repository. The dataset can be authorized using a PXD number: PXD070443 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 15 authors, 2 keywords, 2 funders, 67 references, 24 RRIDs.
Cite
This paper
Song, H., Yang, M., Wu, S., Dai, Q., Qin, W., Xie, W., Chen, Y., Jiang, X., Zhang, X., Deng, X., Ouyang, C., Zhang, Y., Liu, X., Zhu, Y., & Huang, G. (2026). Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling. iScience, 29(6), 116033. https://
BibTeX
@article{song2026androgr
author = {Song, Haochang and Yang, Meng and Wu, Shengquan and Dai, Qihui and Qin, Weihong and Xie, Weiheng and Chen, Yuzhi and Jiang, Xiaoyun and Zhang, Xiaojun and Deng, Xiuqin and Ouyang, Chuang and Zhang, Yunman and Liu, Xinguang and Zhu, Yingjie and Huang, Gonghua},
title = {{Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling}},
journal = {iScience},
year = {2026},
month = may,
volume = {29},
number = {6},
pages = {116033},
publisher = {Elsevier},
issn = {2589-0042},
doi = {10.1016/
url = {https://
pmid = {42211120},
pmcid = {PMC13214295}
}
RIS
TY - JOUR
AU - Song, Haochang
AU - Yang, Meng
AU - Wu, Shengquan
AU - Dai, Qihui
AU - Qin, Weihong
AU - Xie, Weiheng
AU - Chen, Yuzhi
AU - Jiang, Xiaoyun
AU - Zhang, Xiaojun
AU - Deng, Xiuqin
AU - Ouyang, Chuang
AU - Zhang, Yunman
AU - Liu, Xinguang
AU - Zhu, Yingjie
AU - Huang, Gonghua
TI - Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling
T2 - iScience
J2 - iScience
PY - 2026
DA - 2026/
VL - 29
IS - 6
SP - 116033
SN - 2589-0042
PB - Elsevier
DO - 10.1016/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1016/
"type": "article-journal",
"title": "Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling",
"container-title": "iScience",
"author": [
{
"family": "Song",
"given": "Haochang"
},
{
"family": "Yang",
"given": "Meng"
},
{
"family": "Wu",
"given": "Shengquan"
},
{
"family": "Dai",
"given": "Qihui"
},
{
"family": "Qin",
"given": "Weihong"
},
{
"family": "Xie",
"given": "Weiheng"
},
{
"family": "Chen",
"given": "Yuzhi"
},
{
"family": "Jiang",
"given": "Xiaoyun"
},
{
"family": "Zhang",
"given": "Xiaojun"
},
{
"family": "Deng",
"given": "Xiuqin"
},
{
"family": "Ouyang",
"given": "Chuang"
},
{
"family": "Zhang",
"given": "Yunman"
},
{
"family": "Liu",
"given": "Xinguang"
},
{
"family": "Zhu",
"given": "Yingjie"
},
{
"family": "Huang",
"given": "Gonghua"
}
],
"container-title-short":
"volume": "29",
"issue": "6",
"page": "116033",
"DOI": "10.1016/
"PMID": "42211120",
"PMCID": "PMC13214295",
"ISSN": "2589-0042",
"publisher": "Elsevier",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
5,
20
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41467-026-74906-z
- Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice.Journal: Nature communicationsIn common: mouse, cellular / molecular, 3 references
- [2] doi:10.1038/s41467-026-74253-z
- Disruption of the brain-spleen axis impairs monocyte-microglia communication and accelerates disease progression in a mouse model of amyloidosis.Journal: Nature communicationsIn common: Alzheimer's / dementia, mouse, cellular / molecular, 2 references
- [3] doi:10.3389/fnagi.2026.1855522
- Astragaloside IV attenuates hypoxia-reoxygenation-in
duced endothelial senescence and vascular inflammation by modulating the NOTCH1/ VCAM-1 axis. Journal: Frontiers in aging neuroscienceIn common: Alzheimer's / dementia, cellular / molecular, 2 references - [4] doi:10.3390/ijms27156964
- Senescence Markers and Associated Transcriptomic Changes Are Expressed at Early Stages of Alzheimer's Neuropathology but Are Not Independently Related to Dementia.Journal: International journal of molecular sciencesIn common: Alzheimer's / dementia, cellular / molecular, 2 references
- [5] doi:10.1038/s41467-026-74904-1
- FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice.Journal: Nature communicationsIn common: mouse, cellular / molecular, 2 references
- [6] doi:10.1038/s41467-026-76156-5 [code]
- Longitudinal analysis reveals myeloid cell contributions to murine neuroPASC pathogenesis.Journal: Nature communicationsIn common: mouse, cellular / molecular, 2 references
- [7] doi:10.1038/s44400-026-00066-y [code]
- A high-throughput, quantitative platform using 2D dissociated human cerebral organoids to model neuroinflammation in Alzheimer's disease.Journal: NPJ dementiaIn common: Alzheimer's / dementia, cellular / molecular, 2 references
- [8] doi:10.1186/s13024-026-00951-3
- Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic advances.Journal: Molecular neurodegenerationIn common: cellular / molecular, 2 references
- [9] doi:10.1172/jci196112
- Aging-dependent microglial heterogeneity worsens outcomes in models of traumatic brain injury.Journal: The Journal of clinical investigationIn common: mouse, 2 references
- [10] doi:10.1177/0271678x261471282 [code]
- Single-cell analysis of microglia and monocyte dynamics uncovers distinct TNF-driven neuroimmune signatures in humans after intracerebral hemorrhage.Journal: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and MetabolismIn common: cellular / molecular, 2 references
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
