相关实验视频

Updated: Jul 23, 2025

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

在阿尔茨海默氏症的疾病中,突触蛋白的纳米级重组

Wang-Hui Zhu^1,2, Xiao-Xu Yang^1,3,4, Xu-Zhuo Gou^1,2

¹Hefei National Research Center for Physical Sciences at the Microscale, CAS Key Laboratory of Brain Function and Disease, Ministry of Education Key Laboratory for Membrane-less Organelles and Cellular Dynamics, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.

Neuropathology and applied neurobiology

|July 18, 2023

概括

阿尔茨海默病 (AD) 破坏突触纳米结构,改变受体组织和传播. 在AD小鼠模型中,密核粉样蛋白斑被确定为AD小鼠模型中这些渐进性变化的关键局部诱导因素.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

突触功能障碍是阿尔茨海默病 (AD) 的一个标志.
突触蛋白的纳米级组织对于突触功能至关重要.
目前尚不清楚AD中的突触蛋白纳米组织是如何受到影响的.

研究的目的:

在AD的细胞和小鼠模型中系统地表征亚突触蛋白组织的改变.
为了研究粉样β (Aβ) 对突触纳米结构的影响.
为了确定AD中突触病理的潜在诱导因素.

主要方法:

使用免疫覆盖和超分辨率的随机光学重建显微镜 (STORM).
对Aβ1-42处理的神经元培养物和来自APP23 AD小鼠模型的皮质部分进行了分析.
进行了对突触蛋白纳米组织的定量检查.

主要成果:

治疗Aβ1-42干扰了后突触支架/受体保留和纳米尺度对齐.
在APP23小鼠中,GluA1受体与野生型小鼠中的纳米集群相比,显示出均的分布和减少的密度.
在APP23小鼠中,前突触RIM1/2和后突触PSD-95之间的跨突触对齐减少了.
这些重组是随着年龄的推进而发生的,并且位于密集核心粉样质斑块附近.

结论:

突触纳米结构在阿尔茨海默病中经历时空重组.
在AD小鼠模型中,密集核心的粉样蛋白斑块作为突触纳米结构重组的局部诱导剂.
这些发现提供了对AD突触病理背后的分子机制的见解.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.粉样化物-β-β 的存在.随机的光学重建显微镜显微镜.超分辨率显微镜的显微镜.突触纳米领域架构的突触纳米领域架构.

更多相关视频

Biochemical Purification and Proteomic Characterization of Amyloid Fibril Cores from the Brain

Biochemical Purification and Proteomic Characterization of Amyloid Fibril Cores from the Brain

Published on: April 28, 2022

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Published on: January 10, 2025

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...

Amyloid Fibrils

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...