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<p>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.</p>

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Garcinone D mitigates amyloid β42-Induced neurotoxicity: unravelling mechanisms of neuroprotection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Hin Yee Thew,
  • Wei Meng Lim,
  • Yong Sze Ong,
  • Lin Kooi Ong,
  • Marie-Odile Parat,
  • Bey Hing Goh,
  • Kooi Yeong Khaw

摘要

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.