Alzheimer’s disease (AD) is a neurodegenerative disease characterized by dementia and memory loss in the elderly population. The amyloid-β peptide (Aβ) is one of the main pathogenic factors in AD and is known to cause damage to neuronal cellular membranes. There is no cure currently available for AD, and new approaches, including preventive strategies, are highly desirable. In this work, we explore the possibility of protecting neuronal membranes from amyloid-induced damage with naturally existing sugar trehalose. Trehalose has been shown to protect plant cellular membranes in extreme conditions and modify Aβ misfolding. We hypothesize that trehalose can protect the neuronal membrane from amyloid toxicity. In this work, we studied the protective effect of trehalose against Aβ1-42-induced damage in model lipid membranes (DPPC/POPC/cholesterol) using atomic force microscopy and black lipid membrane electrophysiology. Our results demonstrate that Aβ1-42 damaged membranes and led to ionic current leakage across these membranes due to the formation of various defects and pores. The presence of trehalose reduced the ion current across membranes caused by Aβ1-42 peptide damage, thus efficiently protecting the membranes. These findings suggest that the trehalose sugar can potentially be useful in protecting neuronal membranes against amyloid toxicity in AD.

中文翻译：

---

利用 BLM 电生理学研究海藻糖对淀粉样蛋白-膜相互作用的保护作用


阿尔茨海默病（AD）是一种神经退行性疾病，其特征是老年人群中出现痴呆和记忆丧失。 β淀粉样肽（Aβ）是AD的主要致病因素之一，已知会导致神经元细胞膜损伤。目前尚无治疗 AD 的方法，因此非常需要新的方法，包括预防策略。在这项工作中，我们探索了用天然存在的海藻糖保护神经元膜免受淀粉样蛋白诱导的损伤的可能性。海藻糖已被证明可以在极端条件下保护植物细胞膜并改变 Aβ 错误折叠。我们假设海藻糖可以保护神经元膜免受淀粉样蛋白毒性。在这项工作中，我们利用原子力显微镜和黑色脂质膜电生理学研究了海藻糖对模型脂质膜（DPPC/POPC/胆固醇）中 Aβ1-42 诱导损伤的保护作用。我们的结果表明，Aβ1-42 会损坏膜，并由于形成各种缺陷和孔而导致离子电流穿过这些膜泄漏。海藻糖的存在减少了Aβ1-42肽损伤引起的跨膜离子电流，从而有效地保护了膜。这些发现表明，海藻糖可能有助于保护神经元膜免受 AD 中淀粉样蛋白毒性的影响。