ArticleScientific reports2025
Garcinone D mitigates amyloid β42-Induced neurotoxicity: unravelling mechanisms of neuroprotection.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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- Erratum issued
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7 authors.
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Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of Aβ42 peptides, which contribute to oxidative stress, apoptosis, and mitochondrial dysfunction in neurons. Garcinone D (GD), a bioactive xanthone derived from mangosteen, has shown promise as a neuroprotective agent; however, its mechanisms of action against Aβ42-induced neurotoxicity remain insufficiently defined. This study examined the protective effects of GD in Aβ42-treated neuronal cells, focusing on key molecular pathways. Our results demonstrate that GD significantly enhances cell viability and stabilizes mitochondrial function while reducing reactive oxygen species and apoptotic markers in Aβ42-treated cells. Additionally, GD activates key antioxidant pathways involving Nrf2 and HO-1, and inhibits caspase activity, thereby demonstrating a multifaceted approach to neuroprotection. These findings suggest that GD could serve as a valuable therapeutic candidate for AD by addressing multiple aspects of cellular damage that contribute to neurodegeneration. By promoting mitochondrial health while modulating oxidative and apoptotic pathways, GD shows potential for advancing therapeutic strategies in neurodegenerative disorders.
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