ArticleCNS neuroscience & therapeutics2025
Aloe-Emodin Improves Mitophagy in Alzheimer's Disease via Activating the AMPK/PGC-1α/SIRT3 Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies.Frontiers in physiology · 2025Pooled it
- Melatonin alleviates mitochondrial damage by regulating SIRT3‑mediated mitochondrial dynamics in granulosa cells under PCOS‑like conditions.Molecular medicine reports · 2026Article
- Bazi Bushen Capsule restores fertility by targeting mitochondrial health in aging endometrium.iMeta · 2026Article
- The Role of PGC-1α in Neurodegenerative Diseases: Molecular Mechanisms, Translational Challenges, and Therapeutic Potential.Molecular neurobiology · 2026Review
- Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Aloe-emodin inhibits p38 MAPK pathway in Alzheimer's disease treatment: a network pharmacology and experimental verification.Journal of molecular histology · 2026Article
- T7 peptide-engineered liposomal Irisin mitigates PND progression through AMPK/PGC-1α signaling: multi-omic evidence of metabolic and epigenetic modulation.Journal of nanobiotechnology · 2026Article
- Modulation of programmed cell death by botanical drugs in Alzheimer's disease: a review from a traditional Chinese medicine perspective.Frontiers in pharmacology · 2026Review
- Aloe emodin attenuates AβOpen medicine (Warsaw, Poland) · 2026Article
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Therapeutic effect of sustained release of aloe emodin via novel grafted polymer in electrospun nanofiber membranes on peritendinous adhesions.Frontiers in bioengineering and biotechnology · 2026Article
- Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025Review
- Multiple Mechanisms and Therapeutic Strategies for the Involvement of AMPK in the Development of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Role of the AMPK/PGC-1α/SIRT3-Mediated Mitochondrial Dysfunction in the Neurotoxicity of Methanol.Molecular neurobiology · 2025Article
- The green healer: an updated review on the phytochemical profile and therapeutic potential ofFrontiers in nutrition · 2025Review
- The mechanism and therapeutic potential of SIRT3 in central nervous system diseases: a review.Frontiers in pharmacology · 2025Review
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6 authors.
Funding
Abstract
backgroundImpaired mitophagy results in the accumulation of defective mitochondria that are unable to be cleared effectively in Alzheimer's disease (AD). Aloe-emodin (AE), a key component of the traditional Chinese medicine Rhubarb, exhibits neuroprotective effects against Alzheimer's disease, though the underlying mechanism remains unclear. Studying aloe-emodin's role in enhancing mitophagy is vital for improving cognitive function and reducing neuronal damage in Alzheimer's disease.
methodsThe APP/PS1 double transgenic mice were adopted as models for AD to assess the effects of aloe-emodin upon cognitive function and its neuroprotective impact on hippocampal neurons. Additionally, we investigated the regulatory mechanisms of proteins within the aforementioned pathway, and the morphological characteristics of mitophagy-related proteins. An AD hippocampal neuron model was developed using Aβ25-35 to evaluate the mitochondrial function, the protein expression of such a pathway and the mitophagy. This approach aims to elucidate the effects and underlying mechanisms of aloe-emodin in relation to AD.
resultsAE activates mitophagy in neurons, improves cognitive dysfunction, reduces hippocampal damage, and alleviates AD symptoms in model mice. AE activates the expression of AMPK, PGC-1α and SIRT3. Increased expression of SIRT3 in mitochondria promotes mitophagy and regulates the function of mitochondrial proteins. When mitochondrial autophagy is enhanced, the expression of Beclin1, LC3, P62, Parkin, and PINK1-related proteins changes. Further in vitro experiments showed that AE can enhance mitochondrial function in Alzheimer's disease cell models. The mitochondrial membrane potential, GSH, ROS and Ca2+ levels gradually recover, alleviating the pathological manifestations of AD. Knocking down SIRT3 leads to increased mitochondrial damage and a reduction in mitophagy in HT22 cells.
conclusionExperimental results show that AE can activate mitophagy through AMPK/PGC-1α/SIRT3 pathway, alleviate cognitive dysfunction in AD, and reduce damage to hippocampal neurons.
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