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

Modeled Long-Term Effects of Psilocybin on Dynamic Activity and Effective Connectivity of Fronto-Striatal-Thalamic Circuits.

Human brain mapping·2026

Same author

A canary in the mind: A single baseline brain scan predicts adolescent depression and anxiety one year later.

medRxiv : the preprint server for health sciences·2026

Same author

Variational autoencoder for explainable seizure onset phases detection.

Journal of neural engineering·2026

Same author

Restoring oscillatory dynamics in Alzheimer's disease: A laminar whole-brain model of serotonergic psychedelic effects.

Network neuroscience (Cambridge, Mass.)·2026

Same author

Schooling Trajectories and the Development of Brain Dynamics: A Comparative Study of Montessori and Traditional Education.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Same author

The Algorithmic Regulator.

Entropy (Basel, Switzerland)·2026

Search research articles

相关实验视频

Updated: Jan 15, 2026

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

拉米纳神经质量模型中的快速内部神经元功能障碍重现了阿尔茨海默病的振荡生物标志物.

Roser Sanchez-Todo^1,2, Borja Mercadal¹, Edmundo Lopez-Sola^1,2

¹Brain Modeling Department, Neuroelectrics Barcelona, Barcelona, Spain.

Human brain mapping

|January 14, 2026

概括

帕尔瓦胺阳性内部神经元功能障碍驱动阿尔茨海默病 (AD) 的早期过度兴奋性. 使用神经质量模型模拟的这种功能障碍准确地预测了AD的进展到低活性,这意味着晚期的神经元损失.

关键词:

阿尔茨海默氏症的疾病是阿尔茨海默氏症.在M/EEG生物标志物中.层状神经质量模型帕瓦胺阳性内部神经元

更多相关视频

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Published on: July 1, 2018

Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice

Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice

Published on: July 31, 2019

相关实验视频

Last Updated: Jan 15, 2026

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

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Published on: July 1, 2018

Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice

Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice

Published on: July 31, 2019

科学领域:

计算神经科学是一种计算神经科学.
神经退行性疾病建模神经退行性疾病建模
电子生理学电子生理学

背景情况:

阿尔茨海默病 (AD) 的进展涉及皮质过度兴奋性转变为低活性.
帕尔瓦胺阳性 (PV) 内核神经元功能障碍和神经元损失,由粉样β (Aβ) 和高酸化 (hp-τ) 驱动,涉及但机制尚不清楚.

研究的目的:

调查PV内部神经元功能障碍与AD中观察到的两相电生理学变化之间的机制联系.
使用计算方法建模与AD相关的神经活动的进展.

主要方法:

开发了一个整合激发性和抑制性群体的层状神经质量模型.
从PV内部神经元到金字塔细胞的突触合被减少,以模拟Aβ诱导的神经毒性.
模型模拟分析了时间频域中的二极体活动,参数变化探索了像hp-τ病理等替代机制.

主要成果:

模拟的PV内部神经元功能障碍复制了AD的双相进展:最初的过激 (高马/α功率),随后是振荡减速和光谱功率降低.
替代机制,如增加的刺激驱动器,并没有重现这种轨迹.
结合金字塔细胞破坏 (hp-τ) 的模型输出与晚期低活性和降低发射率保持一致.

结论:

光伏内部神经元功能障碍是AD早期电生理学障碍的主要驱动因素.
金字塔细胞损失有助于晚期低活性,在AD进展过程中提供激发-抑制不平衡的机制模型.