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唾液酸通过减少阿尔茨海默病小鼠模型中的淀粉样蛋白沉积、神经纤维生成和神经元凋亡来改善认知缺陷。

Sialic Acid Ameliorates Cognitive Deficits by Reducing Amyloid Deposition, Nerve Fiber Production, and Neuronal Apoptosis in a Mice Model of Alzheimer's Disease.

作者信息

Xiao Min, Yao Chuangyu, Liu Fang, Xiang Wei, Zuo Yao, Feng Kejue, Lu Shuhuan, Xiang Li, Li Muzi, Li Xiangyu, Du Xiubo

机构信息

R&D Center, Cabio Biotech (Wuhan) Co., Ltd., No. 999 Gaoxin Rd., Wuhan 430073, China;

Guangdong Provincial Key Laboratory for Plant Epigenetics, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China;

出版信息

NeuroSci. 2021 Dec 24;3(1):28-40. doi: 10.3390/neurosci3010002. eCollection 2022 Mar.

Abstract

(1) Background: As a natural carbohydrate, sialic acid (SA) is helpful for brain development, cognitive ability, and the nervous system, but there are few reports about the effect of SA on Alzheimer's disease (AD). (2) Method: The present study evaluated the effect of SA on cognitive ability, neuronal activity, Aβ formation, and tau hyperphosphorylation in a double transgenic AD (2×Tg-AD) mice model. The 2×Tg-AD mice were randomly divided into four groups: the AD control group, 17 mg/kg SA-treated AD group, 84 mg/kg SA-treated AD group, and 420 mg/kg SA-treated AD group. Mice from all four groups were fed to 7 months of age for the behavioral test and to 9 months of age for the pathological factors investigation. (3) Results: In the Morris water maze, the escape latency significantly decreased on the fifth day in the SA-treated groups. The number of rearing and crossing times in the open field test also increased significantly, compared with the control group. SA treatment significantly reduced amyloid β-peptide (Aβ) and nerve fibers and increased the number of Nissl bodies in the brain of AD mice. (4) Conclusions: SA reduced the neuron damage by reducing Aβ and inhibited tau protein hyperphosphorylation, which improved the cognitive ability and mobility of AD mice.

摘要

(1) 背景:作为一种天然碳水化合物,唾液酸(SA)有助于大脑发育、认知能力和神经系统,但关于SA对阿尔茨海默病(AD)影响的报道较少。(2) 方法:本研究在双转基因AD(2×Tg-AD)小鼠模型中评估了SA对认知能力、神经元活性、Aβ形成和tau蛋白过度磷酸化的影响。将2×Tg-AD小鼠随机分为四组:AD对照组、17 mg/kg SA处理的AD组、84 mg/kg SA处理的AD组和420 mg/kg SA处理的AD组。四组小鼠均饲养至7月龄进行行为测试,9月龄进行病理因素研究。(3) 结果:在莫里斯水迷宫实验中,SA处理组在第5天的逃避潜伏期显著缩短。与对照组相比,旷场试验中的竖毛和穿越次数也显著增加。SA处理显著减少了AD小鼠脑中的淀粉样β肽(Aβ)和神经纤维,并增加了尼氏体数量。(4) 结论:SA通过减少Aβ减轻神经元损伤,并抑制tau蛋白过度磷酸化,从而改善了AD小鼠的认知能力和运动能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32a1/11523747/5cd1773d0980/neurosci-03-00002-g001.jpg

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