在认知无损的自体主导阿尔茨海默病中功能网络的破坏:磁脑图学研究
Anne M van Nifterick1,2,3, Willem de Haan1,3, Cornelis J Stam2,3
1Alzheimer Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC Location VUmc, 1081 HZ Amsterdam, The Netherlands.
Brain communications
|December 23, 2024
概括
早期的阿尔茨海默氏症在认知能力下降之前显示了振荡减速和功能连接的改变. 突变载体中的这些神经生理变化反映了晚期阿尔茨海默氏症,表明早期的大脑网络中断.
科学领域:
- 神经科学是一个神经科学.
- 神经成像是一种神经成像.
- 阿尔茨海默氏症疾病研究研究
背景情况:
- 阿尔茨海默氏病 (AD) 构成了重大的社会负担,但临床前神经生理学变化仍然不明朗.
- 识别早期变化对于及时干预和管理AD影响至关重要.
- 功能性网络枢纽可能在AD的早期阶段表现出选择性漏洞.
研究的目的:
- 研究早期阿尔茨海默病 (EOAD) 临床前阶段的定量神经生理变化.
- 使用磁脑图 (MEG) 探索光谱功率和功能连接的变化.
- 在AD临床前阶段评估大脑网络中的枢纽脆弱性.
主要方法:
- 在具有AD引发突变 (PSEN1/APP) 和匹配对照的认知正常个体中,利用高分辨率的源重建磁脑电图 (MEG) 和匹配的对照.
- 分析了光谱功率 (,α,β波段) 和功能连接 (基于振幅和相位) 以检测激发-抑制不平衡.
- 计算了枢纽中断指数,以评估中央网络区域的脆弱性.
主要成果:
- 突变携带者表现出振荡减速,包括增加的太功率和下降的后部峰值频率和尾α2功率.
- 在阿尔法和β频段观察到全脑功能连接的减少,特别是在周围时枢纽.
- 一个显著的达频段枢纽干扰指数表明了关键大脑区域的功能连接模式的改变.
结论:
- 临床前的神经生理变化,包括振荡减速和功能连接的改变,在自体主导的EOAD中先发生认知障碍.
- 这些观察到的变化与早期兴奋抑制失衡和活动依赖性退化一致.
- 这些发现支持MEG生物标志物在早期AD诊断和干预策略中的潜力.
更多相关视频
08:43Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
Published on: August 7, 2017
7.8K
09:26Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication
Published on: February 6, 2019
18.7K
相关概念视频
01:26Alzheimer's Disease: Overview
1.7K
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...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.7K
01:29Alzheimer Disease l: Introduction
21
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
21
01:23Alzheimer Disease ll: Pathophysiology
35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
01:22Dementia l: Introduction
35
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
35