Evaluating the Molecular Interactions between Type 2 Diabetes Mellitus and Parkinson's Disease: Role of Antidiabetic Drugs as Promising Therapeutics.

IF 4.1 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
ACS Chemical Neuroscience Pub Date : 2025-03-19 Epub Date: 2025-03-05 DOI:10.1021/acschemneuro.4c00819
Irum Waheed, Talal Sikandri, Sumbal Zaheen, Muhammad Mahtab Aslam Khan Khakwani, Zhaowu An, Tingting Liu, Chaoyang Zhu, Jianshe Wei
{"title":"Evaluating the Molecular Interactions between Type 2 Diabetes Mellitus and Parkinson's Disease: Role of Antidiabetic Drugs as Promising Therapeutics.","authors":"Irum Waheed, Talal Sikandri, Sumbal Zaheen, Muhammad Mahtab Aslam Khan Khakwani, Zhaowu An, Tingting Liu, Chaoyang Zhu, Jianshe Wei","doi":"10.1021/acschemneuro.4c00819","DOIUrl":null,"url":null,"abstract":"<p><p>Evidence from previous research demonstrates a relationship between diabetes mellitus (DM) and Parkinson's disease (PD). T2DM is associated with chronic glucose dysregulation, as an etiological factor. It inhibits neuronal function through disrupted insulin signaling and oxidative stress, which ultimately lead to the loss of dopaminergic neurons in the substantia nigra (SN). Interactions between T2DM and PD were analyzed by gene expression, coexpression, and gene set enrichment via NCBI and STRING databases following pathways like KEGG and Reactome. The study identified nine key gene interactions through published literature on different databases and search engines that are involved in the progression of these chronic diseases. Furthermore, some genetic and nongenetic risk factors, gene mutations and environmental factors, are also involved in the progression of T2DM and PD. This review highlights the limitations of currently available drug treatments for these diseases and examines modern therapeutic approaches to address neurodegenerative and metabolic abnormalities. We critically assess the current experimental methodologies aimed at unraveling the pathophysiological mechanisms linking PD and T2DM while addressing the key challenges impeding a comprehensive understanding of the concurrent emergence of these debilitating age-related conditions.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"988-999"},"PeriodicalIF":4.1000,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Chemical Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1021/acschemneuro.4c00819","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/5 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Evidence from previous research demonstrates a relationship between diabetes mellitus (DM) and Parkinson's disease (PD). T2DM is associated with chronic glucose dysregulation, as an etiological factor. It inhibits neuronal function through disrupted insulin signaling and oxidative stress, which ultimately lead to the loss of dopaminergic neurons in the substantia nigra (SN). Interactions between T2DM and PD were analyzed by gene expression, coexpression, and gene set enrichment via NCBI and STRING databases following pathways like KEGG and Reactome. The study identified nine key gene interactions through published literature on different databases and search engines that are involved in the progression of these chronic diseases. Furthermore, some genetic and nongenetic risk factors, gene mutations and environmental factors, are also involved in the progression of T2DM and PD. This review highlights the limitations of currently available drug treatments for these diseases and examines modern therapeutic approaches to address neurodegenerative and metabolic abnormalities. We critically assess the current experimental methodologies aimed at unraveling the pathophysiological mechanisms linking PD and T2DM while addressing the key challenges impeding a comprehensive understanding of the concurrent emergence of these debilitating age-related conditions.

评估2型糖尿病和帕金森病之间的分子相互作用:降糖药物作为有前途的治疗方法的作用
先前的研究证据表明糖尿病(DM)和帕金森病(PD)之间存在关系。作为一个病因因素,T2DM与慢性血糖失调有关。它通过破坏胰岛素信号和氧化应激抑制神经元功能,最终导致黑质(SN)多巴胺能神经元的丧失。通过NCBI和STRING数据库,通过KEGG和Reactome等途径,通过基因表达、共表达和基因集富集分析T2DM和PD之间的相互作用。该研究通过在不同数据库和搜索引擎上发表的文献,确定了与这些慢性疾病进展有关的九个关键基因相互作用。此外,一些遗传和非遗传危险因素,基因突变和环境因素也参与了T2DM和PD的进展。这篇综述强调了这些疾病目前可用的药物治疗的局限性,并探讨了解决神经退行性和代谢异常的现代治疗方法。我们批判性地评估了当前的实验方法,旨在揭示PD和T2DM之间的病理生理机制,同时解决了阻碍全面理解这些衰老相关疾病同时出现的关键挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
ACS Chemical Neuroscience
ACS Chemical Neuroscience BIOCHEMISTRY & MOLECULAR BIOLOGY-CHEMISTRY, MEDICINAL
CiteScore
9.20
自引率
4.00%
发文量
323
审稿时长
1 months
期刊介绍: ACS Chemical Neuroscience publishes high-quality research articles and reviews that showcase chemical, quantitative biological, biophysical and bioengineering approaches to the understanding of the nervous system and to the development of new treatments for neurological disorders. Research in the journal focuses on aspects of chemical neurobiology and bio-neurochemistry such as the following: Neurotransmitters and receptors Neuropharmaceuticals and therapeutics Neural development—Plasticity, and degeneration Chemical, physical, and computational methods in neuroscience Neuronal diseases—basis, detection, and treatment Mechanism of aging, learning, memory and behavior Pain and sensory processing Neurotoxins Neuroscience-inspired bioengineering Development of methods in chemical neurobiology Neuroimaging agents and technologies Animal models for central nervous system diseases Behavioral research
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信