Traditional Chinese medicine for Alzheimer's disease: pathological mechanisms and multi-target interventions.

Authors

Yige Zhang, Rongqiang Song, Jinyan Wang, Bing Chen, Huixin Sun, Xinchen Ren, Lili Ju, Xiaoya Feng, Xuezhen Wang, Gaofeng Qin

Published in

3 Biotech. Volume 16. Issue 10. Pages 449. Epub Sep 27, 2026.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder driven by multiple interconnected pathological mechanisms. This narrative review systematically searched major biomedical databases for relevant literature published between 2015 and 2026, using predefined keywords combined with manual supplementary searches. Two independent reviewers performed a qualitative screening based on relevance, involving the iterative review of titles, abstracts, and full texts. A targeted selection of representative, high-quality studies centered on TCM and AD pathogenesis/mechanisms was then conducted. Ultimately, studies were included in the narrative review for the mechanistic synthesis of TCM against AD. This review summarizes seven core AD mechanisms, including the Aβ cascade, Tau abnormalities, Neuroinflammation, Regulated cell death, Synaptic plasticity impairment, Gut microbiota-brain axis imbalance, and Oxidative stress, and critically discusses the multi‑target interventions of TCM via key molecules such as GSK-3β, BACE1, SIRT1, NF‑κB, NLRP3, PINK1/Parkin, AMPK, BDNF, PSD‑95, and the Nrf2/HO‑1 pathway. GSK‑3β and NF‑κB act as central hubs linking Aβ/Tau pathology to neuroinflammation, while AMPK, SIRT1, and Nrf2/HO‑1 regulate metabolic and redox homeostasis, PINK1/Parkin control mitophagy, and BDNF/PSD‑95 determine synaptic integrity. TCM's therapeutic superiority lies in its simultaneous modulation of this entire hierarchical network, representing a multi‑target strategy that conventional single‑target drugs cannot replicate. By concurrently modulating these distinct yet interacting nodes, TCM establishes a synergistic therapeutic network that reduces Aβ deposition, attenuates Tau hyperphosphorylation, and mitigates neuronal damage, offering a novel direction for future AD research.

PMID:
42802722
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.