Review3 Biotech2026
Traditional Chinese medicine for Alzheimer's disease: pathological mechanisms and multi-target interventions.
Review in 3 Biotech, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.