Nabizadeh Fardin
School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Alzheimer's Disease Institute, Tehran, Iran.
Geroscience. 2025 Feb;47(1):227-246. doi: 10.1007/s11357-024-01339-1. Epub 2024 Sep 30.
Neurodegeneration in Alzheimer's disease (AD) is known to be mostly driven by tau neurofibrillary tangles. However, both tau and neurodegeneration exhibit variability in their distribution across the brain and among individuals, and the relationship between tau and neurodegeneration might be influenced by several factors. I aimed to map local molecular and connectivity characteristics that affect the association between tau pathology and neurodegeneration. The current study was conducted on the cross-sectional tau-PET and longitudinal T1-weighted MRI scan data of 186 participants from the ADNI dataset including 71 cognitively unimpaired (CU) and 115 mild cognitive impairment (MCI) individuals. Furthermore, the normative molecular profile of a region was defined using neurotransmitter receptor densities, gene expression, T1w/T2w ratio (myelination), FDG-PET (glycolytic index, glucose metabolism, and oxygen metabolism), and synaptic density. I found that the excitatory-inhibitory (E:I) ratio, myelination, synaptic density, glycolytic index, and functional connectivity are linked with deviation in the relationship between tau and neurodegeneration. Furthermore, there was spatial similarity between tau pathology and glycolytic index, synaptic density, and functional connectivity across brain regions. The current study demonstrates that the regional susceptibility to tau-related neurodegeneration is associated with specific molecular and connectomic characteristics of the affected neural systems. I found that the molecular and connectivity architecture of the human brain is linked to the different effects of tau pathology on downstream neurodegeneration.
已知阿尔茨海默病(AD)中的神经退行性变主要由tau神经原纤维缠结驱动。然而,tau和神经退行性变在大脑中的分布以及个体之间都存在变异性,并且tau与神经退行性变之间的关系可能受到多种因素的影响。我的目标是绘制影响tau病理与神经退行性变之间关联的局部分子和连接特征。本研究基于来自ADNI数据集的186名参与者的横断面tau-PET和纵向T1加权MRI扫描数据进行,其中包括71名认知未受损(CU)个体和115名轻度认知障碍(MCI)个体。此外,使用神经递质受体密度、基因表达、T1w/T2w比率(髓鞘形成)、FDG-PET(糖酵解指数、葡萄糖代谢和氧代谢)以及突触密度来定义一个区域的正常分子概况。我发现兴奋-抑制(E:I)比率、髓鞘形成、突触密度、糖酵解指数和功能连接与tau和神经退行性变之间关系的偏差有关。此外,tau病理与大脑区域间的糖酵解指数、突触密度和功能连接之间存在空间相似性。本研究表明,对tau相关神经退行性变的区域易感性与受影响神经系统的特定分子和连接组学特征相关。我发现人类大脑的分子和连接结构与tau病理对下游神经退行性变的不同影响有关。