Investigation of human neurodegeneration-related aggregates of beta-amyloid 1-42 (Aβ42) on bdelloid rotifers is a novel interdisciplinary approach in life sciences. We reapplied an organ size-based in vivo monitoring system, exploring the autocatabolism-related alterations evoked by Aβ42, in a glucose-supplemented starvation model. The experientially easy-to-follow size reduction of the bilateral reproductive organ (germovitellaria) in fasted rotifers was rescued by Aβ42, serving as a nutrient source- and peptide sequence-specific attenuator of the organ shrinkage phase and enhancer of the regenerative one including egg reproduction. Recovery of the germovitellaria was significant in comparison with the greatly shrunken form. In contrast to the well-known neurotoxic Aβ42 (except the bdelloids) with specific regulatory roles, the artificially designed scrambled version (random order of amino acids) was inefficient in autocatabolism attenuation, behaving as negative control. This native Aβ42-related modulation of the ‘functionally reversible organ shrinkage’ can be a potential experiential and supramolecular marker of autocatabolism in vivo.

中文翻译：

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神经变性相关的β-淀粉样蛋白在微体内系统中作为自分解代谢的衰减剂

研究人类在与人类神经退行性疾病有关的β-淀粉样蛋白1-42（Aβ42）的轮虫上的聚集是生命科学领域中一种新颖的跨学科方法。我们重新应用了基于器官大小的体内监测系统，在补充葡萄糖的饥饿模型中探索Aβ42引起的与自身代谢相关的改变。禁食型轮虫中双侧生殖器官（germovitellaria）经历了易于遵循的尺寸减小，通过Aβ42得以挽救，它是器官收缩期的营养源和肽序列特异性衰减剂，也是包括蛋在内的可再生器官的增强剂再生产。与萎缩的形式相比，胚芽孢菌的恢复是重要的。与具有特定调节作用的众所周知的神经毒性Aβ42（除扁桃体以外）相反，人工设计的加扰形式（氨基酸的随机顺序）在自动分解代谢方面效率低下，可作为阴性对照。体内。