Department of Neuroscience, University of Torino, Torino, Italy.
Neuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Torino, Italy.
J Alzheimers Dis. 2018;62(3):1241-1245. doi: 10.3233/JAD-170581.
Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that Aβ monomers could have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of oligomers but also of monomers.
淀粉样蛋白-β(Aβ)已被提议作为阿尔茨海默病(AD)的治疗的生物标志物和药物靶点。每种构象形式的 Aβ 对 AD 病理的神经毒性实体和相关性仍存在争议;Aβ 寡聚体被认为是该肽的主要杀伤形式,而单体则被认为参与了生理过程。在这里,我们综述了单体和寡聚体通过自噬和 tau 聚集等 AD 发病机制相关机制介导的一些不同作用。本综述中报道的数据表明,Aβ 单体可能在维持 AD 的发病机制中起主要作用,AD 治疗不仅应集中于清除寡聚体,还应集中于清除单体。