相关实验视频

Updated: Sep 18, 2025

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis

Published on: July 16, 2021

长髓 (Medulla oblongata) 主导的突触密度网络退化在肌缩侧面硬化症中

Ting Zou¹, Manliu Hou², Honghao Han¹

¹The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu 610054, PR China; MOE Key Laboratory for Neuroinformation, High-Field Magnetic Resonance Brain Imaging Key Laboratory of Sichuan Province, University of Electronic Science and Technology of China, Chengdu 610054, PR China.

NeuroImage. Clinical

|June 21, 2025

概括

肌缩性侧面硬化症 (ALS) 涉及突触损失,大脑网络的变化从长髓向新皮质进展. 这种自下而上的模式为ALS进展提供了新的治疗点.

科学领域:

神经科学是一个神经科学.
神经学神经学
脑网络成像脑网络成像

背景情况:

肌缩侧面硬化症 (ALS) 是一种神经退行性疾病,其特征是运动神经元功能障碍.
运动神经元中的突触损失是ALS的一个关键病理特征.
突触网络变化的体内特征及其在ALS中的进展仍然在很大程度上未被探索.

研究的目的:

为了研究ALS患者的突触密度网络连接性.
为了确定ALS中大脑网络内突触损失的渐进序列.

主要方法:

使用SV2A放射性对象[18F]SynVesT-1进行PET成像,对21名ALS患者和25名健康对照进行.
构建了突触密度相似性网络以分析区域间连接.
应用了格兰杰因果分析来开发因果突触共变网络 (cSCN),以确定突触损失的序列.

主要成果:

与对照组相比,ALS患者的突触密度网络连接性降低,特别是涉及长髓,条纹体和额叶,叶和顶叶.
在ALS患者的这些相互连接的大脑区域中观察到显著的突触损失.
因果突触共变网络分析揭示了突触损失的自下而上的进展,起源于长髓,延伸到条形体和新皮质.

结论:

在ALS中,突触退化遵循一个自下而上的模式,主要影响长髓-条形体-新皮质网络.
这种已识别的网络进展为ALS的新型基于网络的治疗策略提供了潜在的目标.

关键词:

肌缩性侧面硬化症 (AMLS) 是一种疾病.因果突触共变网络因果突触共变网络长髓 (Medulla oblongata) 是一个长髓.网络退化网络退化突触密度相似性网络的突触密度相似性网络.

更多相关视频

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

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.

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Cross-bridge Cycle

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.

Parkinson's Disease: Overview

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...

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,...

Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...