Targeting the Nrf2 Signaling Pathway: A Review of Traditional Chinese Medicine for Alzheimer’s Disease
Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily characterized by [Formula: see text]-amyloid (A[Formula: see text]) deposition, Tau protein hyperphosphorylation, and chronic neuroinflammation. Current pharmacological interventions demonstrate limited therapeutic efficacy. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, a pivotal regulator of oxidative stress and neuroinflammation, plays a critical role in AD pathogenesis. Recent studies have revealed that traditional Chinese medicines (TCMs) and their bioactive constituents can modulate the Nrf2 signaling pathway to mitigate oxidative stress, suppress neuroinflammation, enhance A[Formula: see text] clearance, and reduce Tau protein phosphorylation. By doing so, TCMs exert multi-targeted anti-AD effects. This review systematically summarizes the mechanisms and recent advances concerning the active ingredients of Nrf2 pathway-modulating TCMs, herbal medicines, and TCM formulations for the prevention and treatment of AD. Furthermore, it critically evaluates current research limitations and prospects for future research directions to provide a theoretical foundation for the development of novel anti-AD therapeutics derived from TCMs.
Authors
- Hang Hong (ORCID: https://orcid.org/0000-0003-2532-7897)
- Chunlan Tang (ORCID: https://orcid.org/0000-0001-5297-8965)
- Ming Liu (ORCID: https://orcid.org/0000-0002-2730-2143)
- Xi Zhang (ORCID: https://orcid.org/0000-0002-4638-3997)
- Jiayu Ren (ORCID: https://orcid.org/0000-0002-2610-0347)
Institutions
- Ningbo University (CN)
- Ningbo University of Technology (CN)
- Ningbo College of Health Sciences (CN)
- Ningbo University Affiliated Hospital (CN)
Publication Details
- Journal
- The American Journal of Chinese Medicine
- Published
- 2026-06-16
- DOI
- https://doi.org/10.1142/s0192415x26500400
- Primary Topic
- Genomics, phytochemicals, and oxidative stress
- Type
- article
- Field-Weighted Citation Impact
- 0.00