Abstract
Background
Natural medicines have low toxicity, multi-target effects and long-term clinical use. They inhibit amyloid-β (Aβ) deposition, regulate tau phosphorylation, and exert anti-inflammatory and antioxidant activities, matching Alzheimer's disease (AD) complex pathogenesis. Supported by the World Health Organization, they are promising alternatives to current symptomatic AD drugs that cannot stop disease progression.
Objective
AD poses a growing global neurodegenerative burden, but systematic bibliometric analysis of natural medicines against AD remains lacking. This study aimed to reveal research trends, core contributors, hotspots and mechanisms from 1999 to 2025.
Methods
Literature data were retrieved from the Web of Science Core Collection (WOSCC) database (1999–2025) using a combined subject term search strategy. VOSviewer 1.6.20 was used for collaborative network analysis (countries, institutions, authors) and keyword co-occurrence analysis; CiteSpace 6.3.R1 was applied for keyword burst detection.
Results
Global publications on natural medicines against AD showed phased growth: slow growth (1999–2009), rapid growth (2011–2018), and explosive growth (2020–present). China led in publications; India had the strongest international collaboration. Top co-cited journals included
Journal of Ethnopharmacology
, and key cited literatures focused on natural medicines’ anti-AD effects. Keyword analysis revealed core hotspots: oxidative stress, amyloid-beta, neuroinflammation, and emerging technologies. Core anti-AD mechanisms of natural medicines included inhibiting Aβ aggregation, regulating tau phosphorylation, anti-neuroinflammation, and gut-brain axis modulation. Numerous typical compounds showed potential but faced slow clinical translation.
Conclusions
China is a core contributor. Research has shifted to molecular mechanisms and clinical translation, with network pharmacology, molecular docking and gut-brain axis as frontiers. Future efforts require interdisciplinary cooperation and large-sample trials.