Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Neurosci Lett. 2013 Feb 8;534:285-8. doi: 10.1016/j.neulet.2012.12.023. Epub 2012 Dec 27.
Alzheimer's disease (AD) is a neurodegenerative disorder that results in cognitive impairment. It has been proposed that deposits of beta-amyloid (Aβ) form the cores of the plaque and, subsequently, induce the activation of GSK-3β and the hyperphosphorylation of tau, resulting in cognitive impairment. Oxidative stress has been proposed to be an important factor in the pathogenesis of AD. Cyanidin 3-O-glucoside (Cy3G) is a neuroprotective antioxidant. However, the effects of Cy3G on cognition are unclear. In this paper, we show that Cy3G is protective against the Aβ-induced impairment of learning and memory, but has no effect on normal learning and memory. Moreover, we found that Gy3G attenuated the Aβ-induced tau hyperphosphorylation and GSK-3β hyperactivation observed in AD. Taken together, these results demonstrated that Cy3G can rescue the cognitive impairments that are induced by Aβ via the modulation of GSK-3β/tau, suggesting a potential therapeutic role of Cy3G in AD.
阿尔茨海默病(AD)是一种神经退行性疾病,可导致认知障碍。据认为,β-淀粉样蛋白(Aβ)的沉积形成了斑块的核心,并随后诱导 GSK-3β的激活和 tau 的过度磷酸化,导致认知障碍。氧化应激被认为是 AD 发病机制中的一个重要因素。矢车菊素 3-O-葡萄糖苷(Cy3G)是一种神经保护抗氧化剂。然而,Cy3G 对认知的影响尚不清楚。在本文中,我们表明 Cy3G 可防止 Aβ引起的学习和记忆损伤,但对正常学习和记忆没有影响。此外,我们发现 Cy3G 可减轻 AD 中观察到的 Aβ诱导的 tau 过度磷酸化和 GSK-3β过度激活。综上所述,这些结果表明 Cy3G 可以通过调节 GSK-3β/tau 来挽救 Aβ诱导的认知障碍,提示 Cy3G 在 AD 中的潜在治疗作用。