Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction

Author(s): Tianwen Huang, Fang Fang, Limin Chen, Yuangui Zhu, Jing Zhang, Xiaochun Chen, Shirley Shidu Yan

Journal Name: Current Alzheimer Research

Volume 9 , Issue 3 , 2012

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Mitochondrial dysfunction is one of the major pathological changes seen in Alzheimer’s disease (AD). Amyloid beta-peptide (Aβ), a neurotoxic peptide, accumulates in the brain of AD subjects and mediates mitochondrial and neuronal stress. Therefore, protecting mitochondrion from Aβ-induced toxicity holds potential benefits for halting and treating and perhaps preventing AD. Here, we report that administration of ginsenoside Rg1, a known neuroprotective drug, to primary cultured cortical neurons, rescues Aβ-mediated mitochondrial dysfunction as shown by increases in mitochondrial membrane potential, ATP levels, activity of cytochrome c oxidase (a key enzyme associated with mitochondrial respiratory function), and decreases in cytochrome c release. The protective effects of Rg1 on mitochondrial dysfunction correlate to neuronal injury in the presence of Aβ. This finding suggests that ginsenoside Rg1 may attenuate Aβ-induced neuronal death through the suppression of intracellular mitochondrial oxidative stress and may rescue neurons in AD.

Keywords: Alzheimer’s disease, oligomeric beta-amyloid peptide1-42, mitochondria, ginsenoside Rg1

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Article Details

Year: 2012
Page: [388 - 395]
Pages: 8
DOI: 10.2174/156720512800107636
Price: $65

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