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Evaluating resting-state BOLD variability in relation to biomarkers of preclinical Alzheimer disease
Neurobiology of Aging ( IF 4.2 ) Pub Date : 2020-12-01 , DOI: 10.1016/j.neurobiolaging.2020.08.007
Peter R Millar 1 , Beau M Ances 2 , Brian A Gordon 3 , Tammie L S Benzinger 4 , Anne M Fagan 5 , John C Morris 5 , David A Balota 1
Affiliation  

Recent functional magnetic resonance imaging studies have demonstrated that moment-to-moment variability in the blood oxygen level-dependent (BOLD) signal is related to age differences, cognition, and symptomatic Alzheimer's disease (AD). However, no studies have examined BOLD variability in the context of preclinical AD. We tested relationships between resting-state BOLD variability and biomarkers of amyloidosis, tauopathy, and neurodegeneration in a large (N = 321), well-characterized sample of cognitively normal adults (age = 39-93), using multivariate machine learning techniques. Furthermore, we controlled for cardiovascular health factors, which may contaminate resting-state BOLD variability estimates. BOLD variability, particularly in the default mode network, was related to cerebrospinal fluid (CSF) amyloid-β42 but was not related to CSF phosphorylated tau-181. Furthermore, BOLD variability estimates were also related to markers of neurodegeneration, including CSF neurofilament light protein, hippocampal volume, and a cortical thickness composite. Notably, relationships with hippocampal volume and cortical thickness survived correction for cardiovascular health and also contributed to age-related differences in BOLD variability. Thus, BOLD variability may be sensitive to preclinical pathology, including amyloidosis and neurodegeneration in AD-sensitive areas.

中文翻译:

评估与临床前阿尔茨海默病生物标志物相关的静息状态 BOLD 变异性

最近的功能性磁共振成像研究表明,血氧水平依赖性 (BOLD) 信号的瞬时变化与年龄差异、认知和症状性阿尔茨海默病 (AD) 相关。然而,没有研究检查临床前 AD 背景下的 BOLD 变异性。我们使用多变量机器学习技术在一个大的(N = 321)、特征明确的认知正常成年人(年龄 = 39-93)样本中测试了静息状态 BOLD 变异性与淀粉样变性、tau蛋白病变和神经变性的生物标志物之间的关系。此外,我们控制了心血管健康因素,这些因素可能会污染静息状态 BOLD 变异性估计。大胆的可变性,特别是在默认模式网络中,与脑脊液 (CSF) 淀粉样蛋白-β42 有关,但与 CSF 磷酸化 tau-181 无关。此外,BOLD 变异性估计值还与神经退行性变的标志物有关,包括 CSF 神经丝轻蛋白、海马体积和皮质厚度复合物。值得注意的是,与海马体积和皮质厚度的关系在心血管健康校正后幸存下来,并且还导致了 BOLD 变异性的年龄相关差异。因此,BOLD 变异性可能对临床前病理敏感,包括 AD 敏感区域的淀粉样变性和神经变性。与海马体积和皮质厚度的关系在心血管健康校正后幸存下来,并且还导致了 BOLD 变异性的年龄相关差异。因此,BOLD 变异性可能对临床前病理敏感,包括 AD 敏感区域的淀粉样变性和神经变性。与海马体积和皮质厚度的关系在心血管健康校正后幸存下来,并且还导致了 BOLD 变异性的年龄相关差异。因此,BOLD 变异性可能对临床前病理敏感,包括 AD 敏感区域的淀粉样变性和神经变性。
更新日期:2020-12-01
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