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

Alzheimer's Disease: Overview

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...

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

The <i>NORAD</i> -pumilio regulatory axis links lncRNA dysregulation to tau propagation-associated phenotypes.

bioRxiv : the preprint server for biology·2026

Same author

Understanding Love in Couple Relationships: A Scoping Review of Sternberg's Triangular Theory.

Psychological reports·2026

Same author

Histologically validated diffusion MRI signatures of neuroinflammation and neurodegeneration in Alzheimer disease.

medRxiv : the preprint server for health sciences·2026

Same author

Sex-biased Genetic Risk Loci and Causal Brain Proteins in Parkinson's Disease.

medRxiv : the preprint server for health sciences·2026

Same author

Blood-based circular RNAs for early diagnosis of Alzheimer's disease.

Nature medicine·2026

Same author

A TAD-informed aging-brain xQTL atlas of multi-modal and cell-type-resolved regulatory variation.

medRxiv : the preprint server for health sciences·2026

Search research articles

相关实验视频

Updated: May 17, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

免疫检查点TIM-3调节小质细胞和阿尔茨海默病

Kimitoshi Kimura^1,2,3,4, Ayshwarya Subramanian^1,2,3,5, Zhuoran Yin^1,2,3,6

¹The Gene Lay Institute of Immunology and Inflammation, Brigham and Women's Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

|April 9, 2025

概括

此摘要是机器生成的。

免疫检查点TIM-3 (HAVCR2) 通过TGFβ信号维持大脑微质稳定. 在微质中删除TIM-3会恶化类似阿尔茨海默氏症的病理,但会增强细胞,这表明它具有治疗潜力.

更多相关视频

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

相关实验视频

Last Updated: May 17, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

科学领域:

神经免疫学
细胞生物学
神经退行性疾病

背景情况:

微细胞是参与神经发育和神经炎症的关键脑免疫细胞.
TIM-3 (HAVCR2) 是阿尔茨海默病的遗传风险因素,但其在微质中的作用尚不清楚.
了解微质功能对于神经退行性疾病研究至关重要.

研究的目的:

研究微质中免疫检查点分子TIM-3的功能.
阐明TIM-3影响微质平衡和阿尔茨海默病病理学的机制.
探索向微质TIM-3的治疗潜力.

主要方法:

使用小鼠模型研究微质中的TIM-3表达和功能.
研究了TIM-3与TGFβ信号通路组件的相互作用 (SMAD2,TGFBR2).
使用微质中Havcr2的遗传删除,并分析了5×FAD小鼠对微质表型,认知功能和粉样β病理的影响.
进行单核和单细胞RNA测序以分析微质基因表达.

主要成果:

TGFβ信号诱导微质中的TIM-3表达,从而增强TGFβ信号以维持微质平衡.
微质中Havcr2的遗传删除增加了细胞活动,并促进了神经退行性微质表型 (MGnD/ DAM).
在小鼠阿尔茨海默病模型中,微细胞特异的Havcr2丧失改善了认知缺陷并减少了粉样β病理.
单细胞转录组显示,在缺乏TIM-3的微质中,基因表达转向了前细胞和抗炎性基因表达.

结论:

通过与TGFβ信号通路的相互作用,TIM-3在维持微质平衡方面发挥着至关重要的作用.
针对微质TIM-3是一种潜在的阿尔茨海默病治疗策略.
调节微质中的TIM-3会影响其细胞和炎症功能,从而影响疾病的进展.