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Fractional anisotropy of cerebral white matter and thickness of cortical gray matter across the lifespan.

机译:整个寿命期间脑白质的分数各向异性和皮质灰质的厚度。

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We examined age trajectories of fractional anisotropy (FA) of cerebral white matter (WM) and thickness of cortical gray matter (GM) in 1031 healthy human subjects (aged 11-90 years). Whole-brain FA and GM thickness values followed quadratic trajectories with age but the relationship between them was linear, indicating that a putative biological mechanism may explain the non-linearity of their age trajectories. Inclusion of the FA values into the quadratic model of the whole-brain and regional GM thickness changes with age made the effect of the age(2) term no longer significant for the whole-brain GM thickness and greatly reduced its significance for regional GM thickness measurements. The phylogenetic order of cerebral myelination helped to further explain the intersubject variability in GM thickness. FA values for the early maturing WM were significantly better (p=10(-6)) at explaining variability in GM thickness in maturing (aged 11-20) subjects than FA values for the late maturing WM. The opposite trend was observed for aging subjects (aged 40-90) where FA values for the late maturing WM were better (p=10(-16)) at explaining the variability in GM thickness. We concluded that the non-linearity of the age trajectory for GM thickness, measured from T1-weighted MRI, was partially explained by the heterogeneity and the heterochronicity of the age-related changes in the microintegrity of cerebral WM. We consider these findings as the evidence that the measurements of age-related changes in GM thickness and FA are driven, in part, by a common biological mechanism, presumed to be related to changes in cerebral myelination.
机译:我们检查了1031名健康人(11-90岁)的脑白质(WM)的分数各向异性(FA)和皮质灰质(GM)厚度的年龄轨迹。全脑FA和GM厚度值随年龄变化遵循二次轨迹,但它们之间的关系是线性的,这表明推测的生物学机制可能解释了其年龄轨迹的非线性。将FA值包括在全脑和区域GM厚度随年龄的二次模型中,使得age(2)项对全脑GM厚度的影响不再显着,大大降低了其对区域GM厚度的重要性测量。脑髓鞘形成的系统发育顺序有助于进一步解释受试者间GM厚度的变异性。早熟WM的FA值比晚熟WM的FA值在解释成熟(11-20岁)受试者的GM厚度变异性方面要好得多(p = 10(-6))。对于衰老的受试者(40-90岁)观察到相反的趋势,其中晚期WM的FA值更好地解释了GM厚度的变化(p = 10(-16))。我们得出的结论是,根据T1加权MRI测得的GM厚度年龄轨迹的非线性部分地由大脑WM的微完整性的年龄相关变化的异质性和异时性解释。我们认为这些发现是证据,表明年龄相关的GM厚度和FA变化的测量部分是由一种共同的生物学机制驱动的,该生物学机制被认为与脑髓鞘的改变有关。

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