The role of vascular endothelial growth factor in neurodegeneration and cognitive decline: exploring interactions with biomarkers of Alzheimer disease.
The role of vascular endothelial growth factor in neurodegeneration and cognitive decline: exploring interactions with biomarkers of Alzheimer disease.
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血管内皮生长因子在神经退行性和认知下降中的作用：探索与阿尔茨海默氏病的生物标志物的相互作用。
DOI：
10.1001/jamaneurol.2014.4761
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发表时间：
2015-05
期刊：
影响因子：
29
通讯作者：
Jefferson, Angela L.
中科院分区：
文献类型：
--
作者：
Hohman, Timothy J.;Bell, Susan P.;Jefferson, Angela L.
一部分老年人死后出现阿尔茨海默病(AD)的病理特征，但没有任何明显的痴呆症临床表现。血管内皮生长因子(VEGF)被认为与延缓AD相关的神经退行性变有关。评估血管内皮生长因子水平是否与脑老化结果(海马体体积、认知)相关。进一步评估血管内皮生长因子是否改变AD生物标志物和脑老化结果之间的关系。使用阿尔茨海默病神经成像倡议(ADNI)的神经成像和神经心理学结果进行生物标记物分析。北美地区的前瞻性纵向研究。参与者来自ADNI，包括认知正常(n=90)、轻度认知障碍(n=130)和阿尔茨海默病(n=59)个体。脑脊液(CSF)中的血管内皮生长因子与脑老化结果(海马体体积、情景记忆、执行功能)的横截面相关使用一般线性模型，纵向使用混合效应回归。AD生物标记物(脑脊液淀粉样蛋白-β42和总tau)x血管内皮生长因子的交互作用评估了在存在增强的AD生物标记物的情况下，血管内皮生长因子对脑老化结果的影响。血管内皮生长因子与基线海马区体积(p=0.009)、纵向海马区萎缩(p=0.01)、纵向记忆减退(p<；0.0001)和执行功能(p=0.003)相关。血管内皮生长因子和tau蛋白在预测纵向海马区萎缩(p<；0.0001)、记忆力下降(p=0.01)和执行功能下降(p=0.0002)方面存在交互作用。血管内皮生长因子与淀粉样蛋白β42在预测纵向记忆衰退方面存在交互作用(p=0.0 1)。脑脊液中高水平的血管内皮生长因子与体内更适宜的脑老化有关。当存在增强的AD生物标志物时，神经保护作用最强，这表明血管内皮生长因子可能对表现出AD级联早期特征的个体特别有益。未来的工作应评估体外表达的血管内皮生长因子和病理负担之间的相互作用，以解决潜在的机制。
A subset of older adults present post-mortem with Alzheimer’s disease (AD) pathologic features but without any significant clinical manifestation of dementia. Vascular endothelial growth factor (VEGF) has been implicated in staving off AD-related neurodegeneration. Evaluate whether VEGF levels are associated with brain aging outcomes (hippocampal volume, cognition). Further evaluate whether VEGF modifies relations between AD biomarkers and brain aging outcomes. Biomarker analysis using neuroimaging and neuropsychological outcomes from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Prospective longitudinal study across North America. Participants were drawn from the ADNI and included individuals with normal cognition (n=90), mild cognitive impairment (n=130), and AD (n=59). Cerebrospinal fluid (CSF) VEGF was cross-sectionally related to brain aging outcomes (hippocampal volume, episodic memory, executive function) using a general linear model and longitudinally using mixed-effects regression. AD biomarker (CSF amyloid-β42 and total tau) x VEGF interactions evaluated the effect of VEGF on brain aging outcomes in the presence of enhanced AD biomarkers. VEGF was associated with baseline hippocampal volume (p=0.009), longitudinal hippocampal atrophy (p=0.01), and longitudinal decline in memory (p<0.0001) and executive function (p=0.003). VEGF interacted with tau in predicting longitudinal hippocampal atrophy (p<0.0001), memory decline (p=0.01), and executive function decline (p=0.0002). VEGF interacted with amyloid-β42 in predicting longitudinal memory decline (p=0.01). Elevated CSF VEGF was associated with more optimal brain aging in vivo. The neuroprotective effect appeared strongest in the presence of enhanced AD biomarkers, suggesting that VEGF may be particularly beneficial in individuals showing early hallmarks of the AD cascade. Future work should evaluate the interaction between VEGF expression in vitro and pathologic burden to address potential mechanisms.
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