Zinc deficiency is reported to be a global problem that affects cognitive function. The mechanism underlying zinc deficiency-induced impairment of cognitive function is still obscure. In this study, we treated KM mice (Kun Ming mice) with zinc chelator TPEN (N,N,N',N'-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine) by i.p. injection. NOR (New Object Recognition) tests demonstrated that TPEN can impair the cognitive function of KM mice. Disruption of the GRASP55/Golgin45 complex, and even the Golgi apparatus, was also observed in hippocampus cells by TPEN treatment. Further investigation by IHF showed that enrichment of Aβ peptides occurs in neurons of the cerebral tissue of mice, suggesting that amyloidosis may mediate TPEN-induced impairment of cognitive function. This research not only clarifies that zinc plays an important role in Golgi organization in vivo, but also gives us a possible novel pathway underlying AD development.

中文翻译：

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高尔基体的破坏介导了锌缺乏引起的小鼠认知功能损害。

锌缺乏据报道是影响认知功能的全球性问题。锌缺乏引起的认知功能障碍的机制仍不清楚。在这项研究中，我们通过ip注射用锌螯合剂TPEN（N，N，N'，N'-四（2-吡啶基甲基）-1,2-乙二胺）处理KM小鼠（昆明小鼠）。NOR（新对象识别）测试表明，TPEN可以损害KM小鼠的认知功能。通过TPEN处理，在海马细胞中也观察到了GRASP55 / Golgin45复合物甚至高尔基体的破坏。通过IHF的进一步研究表明，Aβ肽的富集发生在小鼠大脑组织的神经元中，这表明淀粉样变性可能介导TPEN诱导的认知功能损害。