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Copper induces the accumulation of amyloid-beta in the brain

机译：铜诱导大脑中淀粉样β的积累

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Accumulation of amyloid beta protein (Aβ) plays a major role in the etiology of Alzheimer’s disease (AD). Aβ is generated from the cleavage of amyloid precursor protein (APP) by beta-site APP-cleaving enzyme 1 (BACE1). There are two factors that reduce of Aβ accumulation in the brain; degradation by peptidases such as neprilysin (NEP) and clearance via two transporters. The low-density lipoprotein receptor related protein 1 (LRP1) is the major transporter that clears Aβ from brain to blood and the receptor for advanced glycation end products (RAGE) is a receptor that transports Aβ from blood to brain. Copper (Cu) has been postulated to play a role in the pathogenesis of AD, especially involved in Aβ aggregation and toxicity. According to a recent study, Cu(II) could reduce Aβ clearance from the brain in cholesterol-fed rabbits. However, the critical mechanism is unclear. This study was purposed to demonstrate whether Cu (II) would alter accumulation of Aβ in brain. We treated 25 and 50 μM CuSO4 for 48-hour in the well-defined neurodevelopmental cell line (PC12), rat choroidal epithelial cell line (Z310), and rat brain endothelial cell line (RBE4) to estimate the effects on Cu(II) exposure in the brain.
机译：淀粉样β蛋白（Aβ）的积累在阿尔茨海默氏病（AD）的病因中起着重要作用。 Aβ是由β-位点APP裂解酶1（BACE1）裂解淀粉样前体蛋白（APP）产生的。有两个因素可以减少大脑中Aβ的积累；肽酶（如脑啡肽酶（NEP））降解并通过两个转运蛋白清除。低密度脂蛋白受体相关蛋白1（LRP1）是将Aβ从大脑清除到血液的主要转运蛋白，晚期糖基化终产物（RAGE）的受体是将Aβ从血液转移到大脑的受体。铜（Cu）已被假定在AD的发病机理中起作用，尤其是与Aβ聚集和毒性有关。根据最近的一项研究，在胆固醇喂养的兔子中，Cu（II）可以减少大脑中Aβ的清除。但是，关键机制尚不清楚。这项研究旨在证明铜（II）是否会改变大脑中Aβ的积累。我们在定义明确的神经发育细胞系（PC12），大鼠脉络膜上皮细胞系（Z310）和大鼠脑内皮细胞系（RBE4）中处理了25和50μMCuSO4 48小时，以评估对Cu（II）的影响暴露在大脑中。

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