Department of Pharmacology, Tokyo Medical University, Tokyo, Japan.
J Alzheimers Dis. 2011;24 Suppl 2:27-32. doi: 10.3233/JAD-2011-102076.
Despite a bulk of evidence supporting the idea that increased neurotoxic insults lead to Alzheimer's disease (AD), the possibility still remains that insufficiency of an endogenous defense system contributes to the disease progression. Humanin is a bioactive peptide that is likely to inhibit both neuronal death and dysfunction only related to AD by binding to a Humanin receptor on the cell-surface and by activating a STAT3-mediated signal, preventing the onset of dementia. A couple of recent studies presented evidence suggesting that the Humanin signal is decreased in neurons of AD patients. If this is the case, the restoration or activation of the Humanin signal in neurons may change the course of AD.
尽管大量证据支持这样一种观点，即神经毒性损伤的增加会导致阿尔茨海默病（AD），但仍然存在一种可能性，即内源性防御系统的不足可能会导致疾病的进展。人源神经保护因子是一种具有生物活性的肽，它可能通过与细胞表面的人源神经保护因子受体结合并激活 STAT3 介导的信号来抑制仅与 AD 相关的神经元死亡和功能障碍，从而阻止痴呆的发生。最近的几项研究提供的证据表明，AD 患者神经元中的人源神经保护因子信号减少。如果是这样的话，那么恢复或激活神经元中的人源神经保护因子信号可能会改变 AD 的病程。
