Insulin-like growth factor binding protein-2 interactions with Alzheimer's disease biomarkers.
Insulin-like growth factor binding protein-2 interactions with Alzheimer's disease biomarkers.
复制标题
DOI：
10.1007/s11682-016-9636-0
复制
发表时间：
2017-12
影响因子：
3.2
通讯作者：
Alzheimer’s Disease Neuroimaging Initiative
中科院分区：
文献类型：
--
作者：
Lane EM;Hohman TJ;Jefferson AL;Alzheimer’s Disease Neuroimaging Initiative
胰岛素样生长因子结合蛋白-2（IGFBP-2）的血浆水平与阿尔茨海默病（AD）和脑萎缩相关。一些证据表明IGFBP-2和AD神经病理学对神经变性的潜在协同作用，而其他证据表明IGFBP-2对神经变性的作用独立于AD神经病理学。因此，本研究探讨了血浆IGFBP-2和脑脊液（CSF）AD神经病理学生物标志物对海马体积和认知功能的相互作用。访问了AD神经影像学倡议数据（n=354，75±7岁，38%女性），包括血浆IGFBP-2、CSF总tau、CSF Aβ-42、MRI量化的海马体积和神经心理学表现。混合效应回归模型评估了IGFBP-2和AD生物标志物对海马体积和神经心理学表现的相互作用，调整了年龄，性别，教育，APOE ε4状态和认知诊断。观察到IGFBP-2和CSF Aβ-42之间的基线相互作用与左侧（t（305）=-6.37，p=0.002）和右侧海马体积（t（305）=-7.74，p=0.001）相关。在这两种情况下，较高的IGFBP-2水平与较小的海马体积相关，但仅在淀粉样蛋白阴性个体中。观察到的相互作用表明IGFBP-2通过独立于AD神经病理学的单独途径驱动神经变性。
Plasma levels of insulin-like growth factor binding protein-2 (IGFBP-2) have been associated with Alzheimer's disease (AD) and brain atrophy. Some evidence suggests a potential synergistic effect of IGFBP-2 and AD neuropathology on neurodegeneration, while other evidence suggests the effect of IGFBP-2 on neurodegeneration is independent of AD neuropathology. Therefore, the current study investigated the interaction between plasma IGFBP-2 and cerebrospinal fluid (CSF) biomarkers of AD neuropathology on hippocampal volume and cognitive function. AD Neuroimaging Initiative data were accessed (n=354, 75±7 years, 38% female), including plasma IGFBP-2, CSF total tau, CSF Aβ-42, MRI-quantified hippocampal volume, and neuropsychological performances. Mixed effects regression models evaluated the interaction between IGFBP-2 and AD biomarkers on hippocampal volume and neuropsychological performance, adjusting for age, sex, education, APOE ε4 status, and cognitive diagnosis. A baseline interaction between IGFBP-2 and CSF Aβ-42 was observed in relation to left (t(305)=-6.37, p=0.002) and right hippocampal volume (t(305)=-7.74, p=0.001). In both cases, higher IGFBP-2 levels were associated with smaller hippocampal volumes but only among amyloid negative individuals. The observed interaction suggests IGFBP-2 drives neurodegeneration through a separate pathway independent of AD neuropathology.