Molecular mechanisms of amyloid beta metabolism by a cell survival factor

阿尔茨海默病(AD)是导致痴呆症的最常见原因。人素(Human in，HN)是一种新型的神经保护因子，在试管中可抑制AD相关损伤引起的神经元死亡。一种高效的HN衍生物改善了AD小鼠模型的认知缺陷，并维持了淀粉样蛋白负荷的增加，该模型表现出复杂的AD相关病理。在这项研究中，我们研究了HN抑制淀粉样蛋白积累的分子机制，特别是淀粉样蛋白降解酶和胶质细胞清除淀粉样蛋白。

Alzheimer's disease (AD) is the most common cause of dementia. Humanin (HN) is a novel neuroprotective factor and suppresses the neuronal death caused by AD-related insults in test tubes. A highly potent HN derivative ameliorated cognitive deficits and sustained the increase of amyloid burden in an AD mouse model, which exhibits complex AD-relevant pathology. In this study, we investigated the molecular mechanisms how HN suppresses amyloid accumulation, particularly focusing on an amyloid degradation enzyme and amyloid clearance by glial cells.