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功能失调的神经肽网络在散发性阿尔茨海默病发生发展中的加重作用

The Aggravating Role of Failing Neuropeptide Networks in the Development of Sporadic Alzheimer's Disease.

作者信息

Jászberényi Miklós, Thurzó Balázs, Jayakumar Arumugam R, Schally Andrew V

机构信息

Department of Pathophysiology, University of Szeged, P.O. Box 427, H-6701 Szeged, Hungary.

Emergency Patient Care Unit, Albert Szent-Györgyi Health Centre, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary.

出版信息

Int J Mol Sci. 2024 Dec 5;25(23):13086. doi: 10.3390/ijms252313086.

DOI:10.3390/ijms252313086
PMID:39684795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11641508/
Abstract

Alzheimer's disease imposes an increasing burden on aging Western societies. The disorder most frequently appears in its sporadic form, which can be caused by environmental and polygenic factors or monogenic conditions of incomplete penetrance. According to the authors, in the majority of cases, Alzheimer's disease represents an aggravated form of the natural aging of the central nervous system. It can be characterized by the decreased elimination of amyloid β and the concomitant accumulation of degradation-resistant amyloid plaques. In the present paper, the dysfunction of neuropeptide regulators, which contributes to the pathophysiologic acceleration of senile dementia, is reviewed. However, in the present review, exclusively those neuropeptides or neuropeptide families are scrutinized, and the authors' investigations into their physiologic and pathophysiologic activities have made significant contributions to the literature. Therefore, the pathophysiologic role of orexins, neuromedins, RFamides, corticotrope-releasing hormone family, growth hormone-releasing hormone, gonadotropin-releasing hormone, ghrelin, apelin, and natriuretic peptides are discussed in detail. Finally, the therapeutic potential of neuropeptide antagonists and agonists in the inhibition of disease progression is discussed here.

摘要

阿尔茨海默病给老龄化的西方社会带来了日益沉重的负担。这种疾病最常以散发性形式出现,可由环境因素、多基因因素或外显不全的单基因状况引起。据作者称,在大多数情况下,阿尔茨海默病是中枢神经系统自然老化的一种加重形式。其特征可能是β-淀粉样蛋白清除减少以及随之而来的抗降解淀粉样斑块积累。在本文中,对导致老年痴呆症病理生理加速的神经肽调节剂功能障碍进行了综述。然而,在本综述中,仅详细审查了那些神经肽或神经肽家族,并且作者对它们的生理和病理生理活性的研究为该文献做出了重大贡献。因此,本文详细讨论了食欲素、神经介素、RF酰胺、促肾上腺皮质激素释放激素家族、生长激素释放激素、促性腺激素释放激素、胃饥饿素、阿片肽和利钠肽的病理生理作用。最后,本文讨论了神经肽拮抗剂和激动剂在抑制疾病进展方面的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a78/11641508/bca9281bfdea/ijms-25-13086-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a78/11641508/b5ceaa2a162f/ijms-25-13086-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a78/11641508/bca9281bfdea/ijms-25-13086-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a78/11641508/b5ceaa2a162f/ijms-25-13086-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a78/11641508/bca9281bfdea/ijms-25-13086-g002.jpg

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