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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >In vivo reduction of amyloid-β by a mutant copper transporter
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In vivo reduction of amyloid-β by a mutant copper transporter

机译：突变铜转运蛋白在体内还原淀粉样蛋白β

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摘要

Cu ions have been suggested to enhance the assembly and pathogenic potential of the Alzheimer's disease amyloid-β (Aβ) peptide. To explore this relationship in vivo, toxic-milk (tx~J) mice with a mutant ATPase7b transporter favoring elevated Cu levels were analyzed in combination with the transgenic (Tg) CRND8 amyloid precursor protein mice exhibiting robust A? deposition. Unexpectedly, TgCRND8 mice homozygous for the recessive tx~J mutation examined at 6 months of age exhibited a reduced number of amyloid plaques and diminished plasma Aβ levels. In addition, homozygosity for tx~J increased survival of young TgCRND8 mice and lowered endogenous CNS Aβ at times before detectable increases in Cu in the CNS. These data suggest that the beneficial effect of the tx~J mutation on CNS Aβ burden may proceed by a previously undescribed mechanism, likely involving increased clearance of peripheral pools of Aβ peptide.
机译：已经建议Cu离子增强阿尔茨海默氏病淀粉样蛋白-β（Aβ）肽的组装和致病潜力。为了在体内探索这种关系，将具有突变的ATPase7b转运蛋白，有利于Cu水平升高的毒性牛奶（tx〜J）小鼠与表现出强健的Aβ3的转基因（Tg）CRND8淀粉样蛋白前体小鼠进行了分析。沉积。出乎意料的是，对于在6个月大时进行隐性tx〜J突变纯合的TgCRND8小鼠，淀粉样斑块数量减少，血浆Aβ水平降低。另外，在CNS中可检测到的Cu增加之前的时间，tx_J的纯合性增加了年轻的TgCRND8小鼠的存活并且降低了内源CNSAβ。这些数据表明，tx_J突变对CNSAβ负担的有益作用可能通过先前未描述的机制进行，可能涉及增加的Aβ肽外周池清除。

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