Novel surface-modified bioresorbable zinc-based stent materials

综述：《锌与β的相互作用及其对脑细胞的毒性》 锌是人体必需的健康元素，是人脑中第二丰富的微量元素。锌代谢紊乱是 与老年人群和阿尔茨海默病(AD)有关，阿尔茨海默病(AD)除了β外还有许多其他危险因素 还有陶。新的证据表明，锌在AD的发病机制中也起着重要作用。 AS Aβ的产生和聚集、tau磷酸化、氧化还原动态平衡和脑源性神经营养 因子(BDNF)信号转导。锌代谢紊乱可作为AD治疗的靶点。然而，在那里 关于锌浓度的变化，以及锌超载或缺锌的影响，目前仍存在争议 AD患者、小鼠模型和细胞系。提供了这些报告研究中的显著差异， 需要更仔细地设计细胞、临床前和临床研究，才能更清楚地描绘出 锌在阿尔茨海默病临床应用前的作用。为此，我们的目标是研究相互作用 锌与Aβ之间的相互作用、锌结合对Aβ聚集的影响以及锌螯合Aβ(ZNAβ)的潜在毒性 包括神经元、小胶质细胞、星形胶质细胞和脑血管细胞在内的各种脑细胞上的物种- 年度补充项目。

Summary: “Zinc-Aβ interaction and its toxicity on brain cells” Zinc is essential for health and is the second abundant trace element in human brain. Zinc dyshomeostasis is implicated in the elderly population and Alzheimer’s disease (AD) which has many other risk factors besides Aβ and tau. Emerging evidence demonstrated that zinc also plays an important role in the pathogenesis of AD such as Aβ production and aggregation, tau phosphorylation, redox homeostasis, and brain-derived neurotrophic factor (BDNF) signaling. Zinc dyshomeostasis could be a therapeutic target for AD treatment. However, there are still controversies on the zinc concentration alteration, and the effect of zinc overload or zinc deficiency in AD patients, mouse models and cell lines. Providing these significant discrepancies across reported studies, more carefully-designed cellular, preclinical and clinical investigations are needed to portray a clearer picture of zinc’s role in AD development before clinical applications. Toward this end, we aim to investigate the interactions between zinc and Aβ, effect of zinc binding on Aβ aggregation, and the potential toxicity of Zn-chelated Aβ (ZnAβ) species on a variety of brain cells including neurons, microglia, astrocytes, and cerebrovascular cells in this one- year supplemental project.