Neurophysiological trajectories in Alzheimer's disease progression.

Neurophysiological trajectories in Alzheimer's disease progression.
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阿尔茨海默病进展的神经生理学轨迹。

DOI:
10.1101/2023.05.18.541379
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发表时间:
2024
期刊:
bioRxiv : the preprint server for biology
影响因子:
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通讯作者:
Nagarajan,SrikantanS
Nagarajan,SrikantanS
中科院分区:
--
文献类型:
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作者:
Kudo,Kiwamu;Ranasinghe,KamaliniG;Morise,Hirofumi;Syed,Faatimah;Sekihara,Kensuke;Rankin,KatherineP;Miller,BruceL;Kramer,JoelH;Rabinovici,GilD;Vossel,Keith;Kirsch,HeidiE;Nagarajan,SrikantanS

文献摘要

相似文献

阿尔茨海默病(AD)的特征在于淀粉样蛋白-β和错误折叠的tau蛋白的积累,其引起突触功能障碍、进行性神经变性和认知下降。改变的神经振荡已经在AD中被一致地证明。然而,AD进展中异常神经振荡的轨迹及其与神经变性和认知衰退的关系尚不清楚。在这里,我们部署了强大的基于事件的测序模型(EBM)来研究AD阶段的远程和局部神经同步的轨迹,从静息态脑磁图估计。delta-theta带神经同步性的增加以及alpha和beta带的减少在EBM的整个阶段显示出渐进的变化。α和β带同步性的降低先于神经变性和认知衰退,表明频率特异性神经元同步性异常是AD病理生理学的早期表现。长距离同步效应大于局部同步,表明涉及大脑多个区域的连接指标具有更高的敏感性。这些结果表明功能性神经元缺陷的演变沿着AD进展的顺序。
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid-β and misfolded tau proteins causing synaptic dysfunction, and progressive neurodegeneration and cognitive decline. Altered neural oscillations have been consistently demonstrated in AD. However, the trajectories of abnormal neural oscillations in AD progression and their relationship to neurodegeneration and cognitive decline are unknown. Here, we deployed robust event-based sequencing models (EBMs) to investigate the trajectories of long-range and local neural synchrony across AD stages, estimated from resting-state magnetoencephalography. The increases in neural synchrony in the delta-theta band and the decreases in the alpha and beta bands showed progressive changes throughout the stages of the EBM. Decreases in alpha and beta band synchrony preceded both neurodegeneration and cognitive decline, indicating that frequency-specific neuronal synchrony abnormalities are early manifestations of AD pathophysiology. The long-range synchrony effects were greater than the local synchrony, indicating a greater sensitivity of connectivity metrics involving multiple regions of the brain. These results demonstrate the evolution of functional neuronal deficits along the sequence of AD progression.