惊喜!维生素B3或可治疗阿尔兹海默症 | PNAS
2018/02/12
维生素B3是人体必需的13种维生素之一。去年,一项为期12年的研究证实,怀孕期间补充微生物B3或能预防严重出生缺陷。现在,科学家们又发现,维生素B3或许还可以治疗阿尔兹海默症,能减缓大脑认知、记忆功能的损伤。


图片来源:网络

维生素B3在阿尔兹海默症领域的应用前景并不是最新发现的事,有研究团队认为,它可以作为一种替代药物,适用于老年痴呆症。数据表明,高剂量的烟酰胺(nicotinamide,也被成为维生素B3)能够逆转阿尔兹海默症相关的记忆损伤。

现在,来自于美国国家老龄化研究所(NIA)的分子医学实验室负责人Vilhelm A. Bohr带领团队专注于探究一种更有效的维生素B3——烟酰胺核苷(NR)对于大脑损伤的积极意义。相关研究成果发表在《PNAS》期刊。


图片来源:PNAS(doi.org/10.1073/pnas.1718819115)

烟酰胺核苷

这种维生素B3“NR”是线粒体内烟酰胺腺嘌呤二核苷酸(NAD+)的有效前体,NAD+是改善线粒体性能和能量代谢的重要细胞辅因子。

通常,痴呆症会损伤患者大脑细胞的DNA修复能力,进而导致细胞线粒体功能紊乱,最终引发神经再生障碍。而NR是维持线粒体健康、干细胞自我复制、神经元应激的关键物质。

NR减缓神经损伤、提高记忆力

Vilhelm A. Bohr将NR添加至阿尔兹海默症小鼠的饮用水中,并设置健康小鼠(不添加NR)作为对照。

3个月后,与对照组相比,接受NR治疗的小鼠大脑内的Tau蛋白、DNA损失显著减少,神经可塑性、学习、记忆功能增强。与此同时,试验组小鼠受损、死亡神经数量相对较少。但是,有意思的是,它们大脑内β-淀粉样蛋白的水平与对照组一样。

接受NR治疗的小鼠在迷宫任务、物体识别等试验中表现更好,这与大脑内积极的生理变化相一致。

研究人员认为,NR有助于提高干细胞自我更新、分化的能力。而且,NR似乎能够减缓、甚至于逆转大脑海马区的损伤。

下一步,研究团队计划深入研究这一改善背后的机制,从而推进维生素B3在阿尔兹海默症防治上的应用进程。

参考资料:

Vitamin B-3 could be used to treat Alzheimer's

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  • NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency

    Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer’s disease (AD), but their role in disease-defining pathology is unclear. We developed a DNA repair-deficient 3xTgAD/Polβ+/− mouse that exacerbates major features of human AD including phosphorylated Tau (pTau) pathologies, synaptic dysfunction, neuronal death, and cognitive impairment. Here we report that 3xTgAD/Polβ+/− mice have a reduced cerebral NAD+/NADH ratio indicating impaired cerebral energy metabolism, which is normalized by nicotinamide riboside (NR) treatment. NR lessened pTau pathology in both 3xTgAD and 3xTgAD/Polβ+/− mice but had no impact on amyloid β peptide (Aβ) accumulation. NR-treated 3xTgAD/Polβ+/− mice exhibited reduced DNA damage, neuroinflammation, and apoptosis of hippocampal neurons and increased activity of SIRT3 in the brain. NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice. In general, the deficits between genotypes and the benefits of NR were greater in 3xTgAD/Polβ+/− mice than in 3xTgAD mice. Our findings suggest a pivotal role for cellular NAD+ depletion upstream of neuroinflammation, pTau, DNA damage, synaptic dysfunction, and neuronal degeneration in AD. Interventions that bolster neuronal NAD+ levels therefore have therapeutic potential for AD.

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