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Green tea catechin EGCG attenuates hippocampal atrophy and cognitive impairment in obesity via autophagy signaling.

Overview

Authors: Kunyi Huang1,2,3, Xin Li1,4, Yujie Chen2, Yiyun Qi1, Weiying Zhang2, Jia Ee Tan2, Jia Ying Chan2, Jiashuo Lu2, Fangyi Hao1,4, Jiayi Shi1,4, Shuting Yan1, Zhenzhen Huang5, Xiaojun Wu3, Qi Xu2, Zhiwei Ma1,6,7
ORCID iDs: Zhiwei Ma
  1. School of Biomedical Engineering, ShanghaiTech University,Shanghai, China
  2. School of Public Health, Shanghai University of Traditional Chinese Medicine,Shanghai, China
  3. State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Shanghai Key Laboratory of Compound Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine,Shanghai, China
  4. School of Life Science and Technology, ShanghaiTech University,Shanghai, China
  5. Laboratory Animal Center, Shanghai University of Traditional Chinese Medicine,Shanghai, China
  6. State Key Laboratory of Advanced Medical Materials and Devices, ShanghaiTech University,Shanghai, China
  7. Shanghai Clinical Research and Trial Center,Shanghai, China
Journal: NPJ science of food, volume 10, issue 1, article 274
Dates: received 6 October 2025; accepted 24 May 2026; published online 4 June 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1038/s41538-026-00914-4 · PMID 42243131 · PMCID PMC13554131 · OpenAlex W7163548892
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: structural MRI / diffusion (modality), human (organism), other condition (population), cellular / molecular (subfield)
Methods: Connectivity, Spectral & time-frequency, Statistics, fMRI & imaging, Physiology & signal measures
Keywords: Diseases, Neuroscience
Topic: Tea Polyphenols and Effects (Pathology and Forensic Medicine, Medicine), according to OpenAlex
Funding: Shanghai University of Traditional Chinese Medicine (SHUTCM-SKL-202503); National Natural Science Foundation of China (82373563); Shanghai Science and Technology Committee (24ZR1451500); ShanghaiTech University
Citations: not cited yet (Europe PMC); 67 references in the paper

Abstract

Obesity is prevalent and linked to cognitive impairment via hippocampal atrophy and insulin resistance. Here, we investigated whether the primary catechin of green tea, epigallocatechin‑3‑gallate (EGCG), could attenuate this neuropathology. Epidemiological analysis of UK Biobank adults with obesity provided an initial clue, showing a positive linear trend between green tea intake and hippocampal volume (p = 0.07). To elucidate the underlying mechanisms, we administered a human‑achievable dose of EGCG (50 mg/kg) to high‑fat diet-fed mice. EGCG treatment significantly reduced body weight and inflammatory signaling while improving insulin sensitivity, attenuating hippocampal atrophy, and mitigating cognitive deficits. Mechanistically, EGCG rescued synaptic structural integrity by suppressing the pro-inflammatory JNK pathway, restoring hippocampal insulin signaling (IRS1/Akt), and stimulating neuronal autophagy through the AMPK/mTOR/ULK1 axis. Together, these data provide translational evidence that EGCG counteracts obesity-linked neurodegeneration by linking metabolic health to hippocampal integrity through the inflammation–insulin–autophagy axis, motivating dietary trials to mitigate cognitive impairment.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

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Data

Datasets cited

Data availability

The UK Biobank datasets analyzed in the current study are not publicly available due to UK Biobank regulations, but they can be requested via the Access Management System at https://ams.ukbiobank.ac.uk/ams/. All other data supporting the findings of this study are included within the article and its Supplementary Information file. Additional mouse MRI datasets analyzed during the current study are available from the corresponding authors upon reasonable request.

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, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 15 authors, 2 keywords, 4 funders, 66 references.

Cite

This paper

Huang, K., Li, X., Chen, Y., Qi, Y., Zhang, W., Tan, J. E., Chan, J. Y., Lu, J., Hao, F., Shi, J., Yan, S., Huang, Z., Wu, X., Xu, Q., & Ma, Z. (2026). Green tea catechin EGCG attenuates hippocampal atrophy and cognitive impairment in obesity via autophagy signaling. NPJ science of food, 10(1), 274. https://doi.org/10.1038/s41538-026-00914-4

BibTeX

@article{huang2026green,
author = {Huang, Kunyi and Li, Xin and Chen, Yujie and Qi, Yiyun and Zhang, Weiying and Tan, Jia Ee and Chan, Jia Ying and Lu, Jiashuo and Hao, Fangyi and Shi, Jiayi and Yan, Shuting and Huang, Zhenzhen and Wu, Xiaojun and Xu, Qi and Ma, Zhiwei},
title = {{Green tea catechin EGCG attenuates hippocampal atrophy and cognitive impairment in obesity via autophagy signaling}},
journal = {NPJ science of food},
year = {2026},
month = jun,
volume = {10},
number = {1},
pages = {274},
publisher = {Nature Publishing Group},
issn = {2396-8370},
doi = {10.1038/s41538-026-00914-4},
url = {https://doi.org/10.1038/s41538-026-00914-4},
pmid = {42243131},
pmcid = {PMC13554131}
}

RIS

TY - JOUR
AU - Huang, Kunyi
AU - Li, Xin
AU - Chen, Yujie
AU - Qi, Yiyun
AU - Zhang, Weiying
AU - Tan, Jia Ee
AU - Chan, Jia Ying
AU - Lu, Jiashuo
AU - Hao, Fangyi
AU - Shi, Jiayi
AU - Yan, Shuting
AU - Huang, Zhenzhen
AU - Wu, Xiaojun
AU - Xu, Qi
AU - Ma, Zhiwei
TI - Green tea catechin EGCG attenuates hippocampal atrophy and cognitive impairment in obesity via autophagy signaling
T2 - NPJ science of food
J2 - NPJ Sci Food
PY - 2026
DA - 2026/06/04
VL - 10
IS - 1
SP - 274
SN - 2396-8370
PB - Nature Publishing Group
DO - 10.1038/s41538-026-00914-4
UR - https://doi.org/10.1038/s41538-026-00914-4
LA - en
ER -

CSL-JSON

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