ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2023
PPARɑ Ligand Caudatin Improves Cognitive Functions and Mitigates Alzheimer's Disease Defects By Inducing Autophagy in Mice Models.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 14 citations in OpenAlex.
- Erjingwan Alleviates Parkinson's Disease via Activation of PPARA-Mediated Autophagy.Applied biochemistry and biotechnology · 2026Article
- The Effects of Drugs on CYP3A Enzyme Activity and Protein Expression Through Ubiquitination Modification Regulation.Basic & clinical pharmacology & toxicology · 2025Article
- Epilepsy and autophagy modulators: a therapeutic split.Autophagy · 2025Review
- Rhynchophylline alleviates cognitive deficits in multiple transgenic mouse models of Alzheimer's disease via modulating neuropathology and gut microbiota.Acta pharmacologica Sinica · 2025Article
- Protective potential of BM-MSC extracted Exosomes in a rat model of Alzheimer's disease.PloS one · 2025Article
- Unveiling the therapeutic potential of caudatin: Structural optimization, pharmacological mechanisms, and therapeutic implications.Frontiers in pharmacology · 2025Review
- Current aspects of targeting cellular senescence for the therapy of neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Regulatory Mechanisms and Therapeutic Implications of Lysosomal Dysfunction in Alzheimer's Disease.International journal of biological sciences · 2025Review
- Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions.Ibrain · 2025Review
- Article
- Aspartame Causes Developmental Defects and Teratogenicity in Zebra Fish Embryo: Role of Impaired SIRT1/FOXO3a Axis in Neuron Cells.Biomedicines · 2024Article
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Authors and funding
20 authors at 7 institutions in 4 countries.
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Abstract
The autophagy-lysosomal pathway (ALP) is a major cellular machinery involved in the clearance of aggregated proteins in Alzheimer disease (AD). However, ALP is dramatically impaired during AD pathogenesis via accumulation of toxic amyloid beta (Aβ) and phosphorylated-Tau (phospho-Tau) proteins in the brain. Therefore, activation of ALP may prevent the increased production of Aβ and phospho-Tau in AD. Peroxisome proliferator-activated receptor alpha (PPARα), a transcription factor that can activate autophagy, and transcriptionally regulate transcription factor EB (TFEB) which is a key regulator of ALP. This suggests that targeting PPARα, to reduce ALP impairment, could be a viable strategy for AD therapy. In this study, we investigated the anti-AD activity of Caudatin, an active constituent of Cynanchum otophyllum (a traditional Chinese medicinal herb, Qing Yang Shen; QYS). We found that Caudatin can bind to PPARα as a ligand and augment the expression of ALP in microglial cells and in the brain of 3XTg-AD mice model. Moreover, Caudatin could activate PPARα and transcriptionally regulates TFEB-augmented lysosomal degradation of Aβ and phosphor-Tau aggregates in AD cell models. Oral administration of Caudatin decreased AD pathogenesis and ameliorated the cognitive dysfunction in 3XTg-AD mouse model. Conclusively, Caudatin can be a potential AD therapeutic agent via activation of PPARα-dependent ALP.
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