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Protective Effects of Pituitary Adenylate Cyclase-Activating Polypeptide and Vasoactive Intestinal Peptide Against Cognitive Decline in Neurodegenerative Diseases.
Frontiers in Cellular Neuroscience ( IF 4.2 ) Pub Date : 2020-06-22 , DOI: 10.3389/fncel.2020.00221
Irene Solés-Tarrés 1 , Núria Cabezas-Llobet 1 , David Vaudry 2 , Xavier Xifró 1
Affiliation  

Cognitive impairment is one of the major symptoms in most neurodegenerative disorders such as Alzheimer’s (AD), Parkinson (PD), and Huntington diseases (HD), affecting millions of people worldwide. Unfortunately, there is no treatment to cure or prevent the progression of those diseases. Cognitive impairment has been related to neuronal cell death and/or synaptic plasticity alteration in important brain regions, such as the cerebral cortex, substantia nigra, striatum, and hippocampus. Therefore, compounds that can act to protect the neuronal loss and/or to reestablish the synaptic activity are needed to prevent cognitive decline in neurodegenerative diseases. Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two highly related multifunctional neuropeptides widely distributed in the central nervous system (CNS). PACAP and VIP exert their action through two common receptors, VPAC1 and VPAC2, while PACAP has an additional specific receptor, PAC1. In this review article, we first presented evidence showing the therapeutic potential of PACAP and VIP to fight the cognitive decline observed in models of AD, PD, and HD. We also reviewed the main transduction pathways activated by PACAP and VIP receptors to reduce cognitive dysfunction. Furthermore, we identified the therapeutic targets of PACAP and VIP, and finally, we evaluated different novel synthetic PACAP and VIP analogs as promising pharmacological tools.



中文翻译:

垂体腺苷酸环化酶激活多肽和血管活性肠肽对神经退行性疾病认知功能下降的保护作用。

认知障碍是大多数神经退行性疾病(例如阿尔茨海默氏病(AD),帕金森氏症(PD)和亨廷顿病(HD))的主要症状之一,影响了全球数百万人。不幸的是,没有治愈或预防这些疾病进展的治疗方法。认知障碍已与重要大脑区域(例如大脑皮层,黑质,纹状体和海马体)的神经元细胞死亡和/或突触可塑性改变有关。因此,需要能够起到保护神经元丢失和/或重新建立突触活性的化合物的作用,以防止神经退行性疾病的认知能力下降。垂体腺苷酸环化酶激活多肽(PACAP)和血管活性肠肽(VIP)是广泛分布于中枢神经系统(CNS)中的两个高度相关的多功能神经肽。PACAP和VIP通过两个常见的受体VPAC1和VPAC2发挥作用,而PACAP还有一个特定的受体PAC1。在这篇综述文章中,我们首先提出了证据,显示了PACAP和VIP可以对抗AD,PD和HD模型中认知衰退的治疗潜力。我们还审查了PACAP和VIP受体激活的主要转导途径,以减少认知功能障碍。此外,我们确定了PACAP和VIP的治疗目标,最后,我们评估了不同的新型合成PACAP和VIP类似物作为有希望的药理工具。PACAP和VIP通过两个常见的受体VPAC1和VPAC2发挥作用,而PACAP还有一个特定的受体PAC1。在这篇综述文章中,我们首先提出了证据,显示了PACAP和VIP可以对抗AD,PD和HD模型中认知衰退的治疗潜力。我们还审查了PACAP和VIP受体激活的主要转导途径,以减少认知功能障碍。此外,我们确定了PACAP和VIP的治疗目标,最后,我们评估了不同的新型合成PACAP和VIP类似物作为有希望的药理工具。PACAP和VIP通过两个常见的受体VPAC1和VPAC2发挥作用,而PACAP还有一个特定的受体PAC1。在这篇综述文章中,我们首先提出了证据,显示了PACAP和VIP可以对抗AD,PD和HD模型中的认知能力下降的治疗潜力。我们还审查了PACAP和VIP受体激活的主要转导途径,以减少认知功能障碍。此外,我们确定了PACAP和VIP的治疗目标,最后,我们评估了不同的新型合成PACAP和VIP类似物作为有希望的药理工具。我们首先提出的证据表明,PACAP和VIP可以对抗AD,PD和HD模型中的认知能力下降的治疗潜力。我们还审查了PACAP和VIP受体激活的主要转导途径,以减少认知功能障碍。此外,我们确定了PACAP和VIP的治疗目标,最后,我们评估了不同的新型合成PACAP和VIP类似物作为有希望的药理工具。我们首先提出的证据表明,PACAP和VIP可以对抗AD,PD和HD模型中的认知能力下降的治疗潜力。我们还审查了PACAP和VIP受体激活的主要转导途径,以减少认知功能障碍。此外,我们确定了PACAP和VIP的治疗目标,最后,我们评估了不同的新型合成PACAP和VIP类似物作为有希望的药理工具。

更新日期:2020-07-17
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