Search research articles

关于 JoVE

概览领导团队博客 JoVE 帮助中心

作者

出版流程编辑委员会范围与政策同行评审常见问题投稿

图书馆员

用户评价订阅访问资源图书馆顾问委员会常见问题

研究

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments 存档

教育

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual 教师资源中心教师网站

使用条款与条件

相关概念视频

Neural Regulation

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序

Same author

Cyanoacetylation of amines <i>via</i> a traceless cyanoacetyl radical: synthetic access to teriflunomide.

Chemical communications (Cambridge, England)·2026

Same author

Organocatalytic Multicomponent Reactions Using 1,1-Diaminobenzalazine: Synthesis of Pyrano[2,3-<i>c</i>]pyrazoles and Pyranochromenes.

The Journal of organic chemistry·2026

Same author

Design and Pictet-Spengler enabled synthesis of carboxamide-substituted imidazo[1,2-<i>a</i>]quinoxalines as dual EGFR and tubulin targeting anticancer agents.

Journal of enzyme inhibition and medicinal chemistry·2026

Same author

Heat Shock Proteins as Cancer Biomarkers: From Mechanism to Clinical Application.

Molecular diagnosis & therapy·2026

Same author

Cyclopropyl-1,1-Dinitrile as a Five-Atom Synthon: Regioselective Ring-Opening and a Keteneimine-Enamine-Based Nitrile-to-Nitrile Condensation Affording an Entry to Pyridines.

The Journal of organic chemistry·2026

Same author

Correction: Nitrenium ion ↔ nitreone resonance in fused cyclic five-membered triazolium ions (<i>f</i>CFTIs): a quantum chemical study.

Physical chemistry chemical physics : PCCP·2026

Search research articles

相关实验视频

Updated: Jan 6, 2026

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

在exanatide调节α-synuclein聚合中的M14替代物.

Venkataharsha Panuganti¹, Kanika Manchanda², Prasad V Bharatam^2,3

¹Department of Biotechnology, National Institute of Pharmaceutical Education and Research, S.A.S. Nagar, Punjab, India.

The FEBS journal

|November 9, 2025

概括

埃克塞纳提德突变体显示出抑制α-synuclein聚合的潜力,这是帕金森病 (PD) 的关键因素. 这些改性可能通过促进细胞存活和自来为神经退行性疾病提供新的治疗途径.

关键词:

帕金森病的疾病.在糖尿病中,糖尿病是血糖类的.脱氧化的使用方法蛋白质聚合蛋白质的聚合物

更多相关视频

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Published on: May 30, 2015

相关实验视频

Last Updated: Jan 6, 2026

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Published on: May 30, 2015

科学领域:

神经科学是一个神经科学.
生物化学生化学
药理学药理学是指药理学的学科.

背景情况:

2型糖尿病 (T2DM) 和帕金森病 (PD) 分享路径失调.
抗糖尿病药物,如埃克西纳提德,在PD模型中显示神经保护作用.
埃克塞纳提德是一种GLP1R激动剂,可以穿过血脑屏障,改善动物的PD症状.

研究的目的:

研究exenatide对α-synuclein聚合的影响.
探索如何修改exenatide的M14位置影响聚合.
在PD模型中评估exenatide突变物的治疗潜力.

主要方法:

在exenatide的M14位置引入了替代突变.
在实验室中进行了对复合人类α-synuclein的聚合测试.
用SH-SY5Y细胞研究聚合和细胞存活.
采用了分子动力学 (MD) 模拟和流细胞计.

主要成果:

单独使用埃克萨纳提德在体外没有影响α-synuclein聚合.
在M14K exenatide突变稳定了α-synuclein并减少了聚合.
所有的exenatide突变物在SH-SY5Y细胞中减弱了α-synuclein聚合,增加了细胞存活率.
类治疗诱导了自,有助于减少蛋白质聚合.

结论:

埃克塞纳提德的M14修饰可以影响α-synuclein稳定性和聚合.
埃克塞纳提德及其突变体在细胞PD模型中表现出神经保护作用.
诱导自是一种关键的机制,可以通过exenatide来减少蛋白质聚合.
埃克塞纳提德突变物需要进一步研究,作为PD治疗的潜在α-synuclein聚合抑制剂.