在临床前阿尔茨海默病中,与粉样蛋白相关的默认模式网络超连接性和网络特异性的纵向下降
Woo-Jin Cha1, Evgeny J Chumin2,3, Dahyun Yi4
1Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|January 30, 2026
概括
阿尔茨海默病 (AD) 研究表明,在认知正常的个体中,粉样β (Aβ) 阳性与增加的默认模式网络 (DMN) 连接性有关. 这种早期的超连接性可能预测了临床前AD的未来大脑网络变化.
科学领域:
- 神经科学是一个神经科学.
- 医疗成像医学成像
- 阿尔茨海默氏症疾病研究研究
背景情况:
- 在阿尔茨海默病 (AD) 连续体中,研究了默认模式网络 (DMN) 功能连接 (FC) 的特定阶段变化.
- 检查了DMN内FC中的早期粉样β (Aβ) 相关变化及其对纵向DMN网络之间的连接 (DMN-FCbetween) 的预测.
研究的目的:
- 为了确定在阿尔茨海默氏病谱中大脑网络内部和大脑网络之间的功能连接如何变化.
- 评估早期的粉样β积累是否影响这些连接模式,并预测未来的变化.
主要方法:
- 分析了来自4个组的396名老年人的静止状态fMRI数据:Aβ阴性CN,Aβ阳性CN,Aβ阳性MCI和Aβ阳性痴呆症.
- 进行横截面和纵向分析 (2年随访) 以比较DMN-FC并评估与Aβ负担的预测关系.
主要成果:
- 与其他组相比,Aβ阳性认知正常 (CN+) 个体表现出高达DMN内FC和降低DMNFCbetween.
- 在认知正常的个体中,基线内-DMN FC预测了DMN-FCbetween的纵向增加,特别是在CN+组.
- 粉样蛋白负担与认知正常个体的FC变化有关,但与认知障碍患者无关.
结论:
- 在DMN中与粉样β相关的超连接性是临床前AD的特征.
- 这种早期的超级连接可能代表了一个漏洞,推动了AD的逐渐网络层次变化.
- 研究结果表明,临床前阿尔茨海默病的DMN变化是Aβ依赖的,并且在认知衰退之前发生.
关键词:
阿尔茨海默病的疾病阿尔茨海默病的疾病.在 KBASE 基础上.氨基βββββββββββββββββββββββββ默认模式网络模式 默认模式网络模式功能连接性的功能连接性超级连接 超级连接 超级连接更多相关视频
06:23The 4 Mountains Test: A Short Test of Spatial Memory with High Sensitivity for the Diagnosis of Pre-dementia Alzheimer's Disease
Published on: October 13, 2016
36.6K
06:23Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
7.1K
相关概念视频
Long-term Depression
27.3K
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.
27.3K
Long-term Depression
2.6K
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...
Calcium Ion Concentration Mechanism
If over...
2.6K
Alzheimer'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
Alzheimer Disease l: Introduction
29
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...
29
Alzheimer Disease ll: Pathophysiology
42
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...
42
Dementia 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
