Chen Xin-Yi, Du Yi-Feng, Chen Lei
Department of Physiology and Pathophysiology, Qingdao University, Qingdao, China.
Department of Neurology, Provincial Hospital Affiliated to Shandong University, Jinan, China.
Front Mol Neurosci. 2019 Jan 11;11:493. doi: 10.3389/fnmol.2018.00493. eCollection 2018.
Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by cognitive deficits and neuronal loss. Deposition of beta-amyloid peptide (Aβ) causes neurotoxicity through the formation of plaques in brains of Alzheimer's disease. Numerous studies have indicated that the neuropeptides including ghrelin, neurotensin, pituitary adenylate cyclase-activating polypeptide (PACAP), neuropeptide Y, substance P and orexin are closely related to the pathophysiology of Alzheimer's disease. The levels of neuropeptides and their receptors change in Alzheimer's disease. These neuropeptides exert neuroprotective roles mainly through preventing Aβ accumulation, increasing neuronal glucose transport, increasing the production of neurotrophins, inhibiting endoplasmic reticulum stress and autophagy, modulating potassium channel activity and hippocampal long-term potentiation. Therefore, the neuropeptides may function as potential drug targets in the prevention and cure of Alzheimer's disease.
阿尔茨海默病(AD)是一种与年龄相关的神经退行性疾病,其特征为认知缺陷和神经元丧失。β-淀粉样肽(Aβ)的沉积通过在阿尔茨海默病患者大脑中形成斑块而导致神经毒性。大量研究表明,包括胃饥饿素、神经降压素、垂体腺苷酸环化酶激活多肽(PACAP)、神经肽Y、P物质和食欲素在内的神经肽与阿尔茨海默病的病理生理学密切相关。神经肽及其受体的水平在阿尔茨海默病中会发生变化。这些神经肽主要通过防止Aβ积累、增加神经元葡萄糖转运、增加神经营养因子的产生、抑制内质网应激和自噬、调节钾通道活性以及海马长时程增强来发挥神经保护作用。因此,神经肽可能作为预防和治疗阿尔茨海默病的潜在药物靶点。