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首页> 外文期刊>Neurobiology of disease >A multifunctional peptide rescues memory deficits in Alzheimer's disease transgenic mice by inhibiting Aβ42-induced cytotoxicity and increasing microglial phagocytosis
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A multifunctional peptide rescues memory deficits in Alzheimer's disease transgenic mice by inhibiting Aβ42-induced cytotoxicity and increasing microglial phagocytosis

机译：多功能肽通过抑制Aβ42诱导的细胞毒性和增加小胶质细胞吞噬作用来挽救阿尔茨海默氏病转基因小鼠的记忆缺陷

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摘要

Alzheimer's disease (AD) is characterized by progressive memory loss due to extracellular senile plaques and intracellular neurofibrillary tangles. The toxic β-amyloid (Aβ) aggregates that form in AD can induce the overproduction of reactive oxygen species (ROS), nitric oxide (NO), and proinflammatory cytokines. These Aβ aggregates likely play a pivotal role in the onset and progression of AD. Reducing Aβ generation, inhibiting Aβ toxicity, and improving Aβ clearance are promising therapeutic strategies for AD. The present paper is the first to reveal a heptapeptide (XD4) isolated from a Ph.D.-C7C library through phage display that significantly inhibited Aβ cytotoxicity, increased the microglial phagocytosis of Aβ, decreased the Aβ-induced generation of ROS and NO, and attenuated the disequilibrium of calcium homeostasis in vitro. Remarkably, XD4 also attenuated memory deficits in β-amyloid precursor protein/presenilin 1 (APPswe/PS1dE9) transgenic mice, and reduced amyloid plaque burden and Aβ40/42 levels. The results of the present study indicate that this peptide, which specifically targets Aβ, may be a promising new therapy for patients exhibiting cognitive impairment and increased Aβ burden.
机译：阿尔茨海默氏病（AD）的特征是由于细胞外老年斑和细胞内神经原纤维缠结导致进行性记忆丧失。在AD中形成的有毒β-淀粉样蛋白（Aβ）聚集体可诱导活性氧（ROS），一氧化氮（NO）和促炎性细胞因子的过量生产。这些Aβ聚集体可能在AD的发作和发展中起关键作用。减少Aβ产生，抑制Aβ毒性和提高Aβ清除率是AD的有前途的治疗策略。本论文首次揭示了通过噬菌体展示从Ph.D.-C7C库中分离出的七肽（XD4），可显着抑制Aβ的细胞毒性，增加Aβ的小胶质细胞吞噬作用，减少Aβ诱导的ROS和NO的产生，并减轻了体外钙稳态的不平衡。值得注意的是，XD4还减轻了β-淀粉样蛋白前体蛋白/早老素1（APPswe / PS1dE9）转基因小鼠的记忆缺陷，并减少了淀粉样斑块负担和Aβ40/ 42水平。本研究的结果表明，这种针对Aβ的肽可能是具有认知障碍和Aβ负担增加的患者的有前途的新疗法。

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