Neurology Clinic, Azienda Ospedaliero Universitaria, Ospedali Riuniti di Ancona, 60126 Ancona, Italy.
Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, 60126 Ancona, Italy.
J Integr Neurosci. 2021 Dec 30;20(4):1059-1065. doi: 10.31083/j.jin2004107.
Vasoactive peptides constitute a heterogenous family of mediators exerting various physiological functions, mostly studied for their vasotropic effects and role as peripheral neurotransmitters/neuromodulators, mainly involved in nociceptive transmission modulation. They have been divided into vasodilatory or vasoconstrictive peptides, according to their predominant effects on vascular tone. Recent research has shown in the Central Nervous System effects as transmitters and "growth factor-like" signals. Therefore, deregulation of their signaling systems has been thought to play a role in neural cell death and in the pathogenesis of neurodegenerative disorders, including Alzheimer's disease, since these peptides can regulate neuronal stress signaling, survival cascades, synaptic plasticity. This review considers evidence about the implication of neuropeptide systems in Alzheimer's disease while focusing mainly on calcitonin gene-related peptide-alpha. In vitro and in vivo studies have shown potential implications in its pathogenesis. It has been possibly proposed as a neuroprotective agent, considering not only its pleiotropic actions on blood vessels, neurovascular coupling, energy metabolism, but also its potential actions on neuronal, glial, and immune system stress signaling, which might also derive from its structural homology to amylin. Amylin signaling is thought to be disrupted in Alzheimer's disease, and amylin itself takes part in the composition of senile plaques. Calcitonin gene-related peptide-containing systems seem more closely related to Alzheimer's disease pathogenesis than other neuropeptidergic systems, and their regulation might represent an interesting mechanism in developing novel therapeutic approaches.
血管活性肽构成了一个具有多种生理功能的介质家族,其作用大多集中在血管张力的改变和作为外周神经递质/神经调质上,主要参与疼痛信号的传递调节。根据其对血管紧张度的主要影响,它们可分为血管舒张肽或血管收缩肽。最近的研究表明,在中枢神经系统中,它们作为递质和“生长因子样”信号发挥作用。因此,人们认为它们信号系统的失调可能在神经细胞死亡和神经退行性疾病(包括阿尔茨海默病)的发病机制中发挥作用,因为这些肽可以调节神经元应激信号、存活级联、突触可塑性。这篇综述考虑了神经肽系统在阿尔茨海默病中的作用的证据,主要集中在降钙素基因相关肽-α上。体外和体内研究表明其在发病机制中有潜在的作用。鉴于其对血管、神经血管耦联、能量代谢的多效作用,以及其对神经元、神经胶质和免疫系统应激信号的潜在作用,它可能被提议作为一种神经保护剂,而不仅仅是其结构同源物淀粉样蛋白。淀粉样蛋白信号被认为在阿尔茨海默病中被破坏,而淀粉样蛋白本身参与了老年斑的组成。降钙素基因相关肽包含的系统与阿尔茨海默病的发病机制似乎更为密切相关,其调节可能代表了开发新治疗方法的一个有趣机制。