PDF(Pubmed)
Abstract：
UNASSIGNED: Brain-derived neurotrophic factor levels are higher in those who are physically active and lower in people with cognitive dysfunction. This study investigated whether brain-derived neurotrophic factor mediated or modified the association of sedentary time to MRI-estimated brain volumes in midlife.
UNASSIGNED: Baseline (n = 612) and five-year follow-up (n = 418) data were drawn from the multicenter Coronary Artery Risk Development in Young Adults Brain MRI sub-study, including Black and White participants (aged 50.3 years, 51.6% females, 38.6% Black). Sedentary time (hours per day) was categorized into quartiles with low ≤ 4.3 (reference) and high > 8.4. Outcomes of the study were total brain, white matter, gray matter, hippocampal volumes, and white matter fractional anisotropy at baseline and 5-year percent change from baseline. The study used general linear regression models to examine the mediation and moderation effects of brain-derived neurotrophic factor (natural log transformed) on the associations of sedentary time to brain outcomes. The authors adjusted the regression model for age, sex, race, intracranial volume, education, and vascular factors.
UNASSIGNED: Cross-sectionally, baseline participants with the highest sedentary time had a lower total brain (-12.2 cc; 95%CI: -20.7, -3.7), gray matter (-7.8 cc; 95%CI: -14.3, -1.3), and hippocampal volume (-0.2 cc; 95%CI: -0.3, 0.0) compared with populations with the lowest sedentary time. The brain-derived neurotrophic factor levels did not mediate the associations between brain measures and sedentary time. Brain-derived neurotrophic factor was found to moderate associations of sedentary time to total brain and white matter volume such that the brain volume difference between high and low sedentary time decreased as brain-derived neurotrophic factor levels increased. Longitudinally, higher baseline brain-derived neurotrophic factor level was associated with less brain volume decline. The longitudinal associations did not differ by sedentary time, and brain-derived neurotrophic factor did not mediate or moderate the association of sedentary time to brain measure changes.
UNASSIGNED: Higher brain-derived neurotrophic factor levels may buffer the negative effects of sedentary time on the brain.
UNASSIGNED: Baseline (n = 612) and five-year follow-up (n = 418) data were drawn from the multicenter Coronary Artery Risk Development in Young Adults Brain MRI sub-study, including Black and White participants (aged 50.3 years, 51.6% females, 38.6% Black). Sedentary time (hours per day) was categorized into quartiles with low ≤ 4.3 (reference) and high > 8.4. Outcomes of the study were total brain, white matter, gray matter, hippocampal volumes, and white matter fractional anisotropy at baseline and 5-year percent change from baseline. The study used general linear regression models to examine the mediation and moderation effects of brain-derived neurotrophic factor (natural log transformed) on the associations of sedentary time to brain outcomes. The authors adjusted the regression model for age, sex, race, intracranial volume, education, and vascular factors.
UNASSIGNED: Cross-sectionally, baseline participants with the highest sedentary time had a lower total brain (-12.2 cc; 95%CI: -20.7, -3.7), gray matter (-7.8 cc; 95%CI: -14.3, -1.3), and hippocampal volume (-0.2 cc; 95%CI: -0.3, 0.0) compared with populations with the lowest sedentary time. The brain-derived neurotrophic factor levels did not mediate the associations between brain measures and sedentary time. Brain-derived neurotrophic factor was found to moderate associations of sedentary time to total brain and white matter volume such that the brain volume difference between high and low sedentary time decreased as brain-derived neurotrophic factor levels increased. Longitudinally, higher baseline brain-derived neurotrophic factor level was associated with less brain volume decline. The longitudinal associations did not differ by sedentary time, and brain-derived neurotrophic factor did not mediate or moderate the association of sedentary time to brain measure changes.
UNASSIGNED: Higher brain-derived neurotrophic factor levels may buffer the negative effects of sedentary time on the brain.
摘要：
■运动活跃者的脑源性神经营养因子水平较高，而认知功能障碍者的脑源性神经营养因子水平较低。这项研究调查了中年人脑源性神经营养因子是否介导或改变了久坐时间与MRI估计的脑容量的关联。
■基线（n=612）和5年随访（n=418）数据来自年轻成年人的多中心冠状动脉风险发展脑MRI子研究，包括黑人和白人参与者(年龄50.3岁，51.6%的女性，38.6%黑色）。久坐时间（每天小时数）分为四分位数，低≤4.3（参考），高>8.4。这项研究的结果是全脑，白质,灰质,海马体积,和白质分数各向异性在基线和5年的变化百分比从基线。该研究使用一般线性回归模型来检查脑源性神经营养因子（自然对数转换）对久坐时间与大脑结局的关联的调解和调节作用。作者调整了年龄回归模型，性别,种族,颅内容积,教育,和血管因素。
■横截面，久坐时间最长的基线参与者的总脑较低（-12.2cc;95CI：-20.7，-3.7），灰质（-7.8cc；95CI：-14.3，-1.3），与久坐时间最低的人群相比，海马体积（-0.2cc；95CI：-0.3，0.0）。脑源性神经营养因子水平并未介导大脑测量与久坐时间之间的关联。发现脑源性神经营养因子可调节久坐时间与总脑和白质体积的关联，从而随着脑源性神经营养因子水平的升高，高久坐时间和低久坐时间之间的脑体积差异降低。纵向,较高的基线脑源性神经营养因子水平与较少的脑容量下降相关.纵向关联在久坐时间上没有差异，脑源性神经营养因子不能介导或缓和久坐时间与大脑测量变化的关联。
■较高的脑源性神经营养因子水平可能会缓冲久坐时间对大脑的负面影响。
■基线（n=612）和5年随访（n=418）数据来自年轻成年人的多中心冠状动脉风险发展脑MRI子研究，包括黑人和白人参与者(年龄50.3岁，51.6%的女性，38.6%黑色）。久坐时间（每天小时数）分为四分位数，低≤4.3（参考），高>8.4。这项研究的结果是全脑，白质,灰质,海马体积,和白质分数各向异性在基线和5年的变化百分比从基线。该研究使用一般线性回归模型来检查脑源性神经营养因子（自然对数转换）对久坐时间与大脑结局的关联的调解和调节作用。作者调整了年龄回归模型，性别,种族,颅内容积,教育,和血管因素。
■横截面，久坐时间最长的基线参与者的总脑较低（-12.2cc;95CI：-20.7，-3.7），灰质（-7.8cc；95CI：-14.3，-1.3），与久坐时间最低的人群相比，海马体积（-0.2cc；95CI：-0.3，0.0）。脑源性神经营养因子水平并未介导大脑测量与久坐时间之间的关联。发现脑源性神经营养因子可调节久坐时间与总脑和白质体积的关联，从而随着脑源性神经营养因子水平的升高，高久坐时间和低久坐时间之间的脑体积差异降低。纵向,较高的基线脑源性神经营养因子水平与较少的脑容量下降相关.纵向关联在久坐时间上没有差异，脑源性神经营养因子不能介导或缓和久坐时间与大脑测量变化的关联。
■较高的脑源性神经营养因子水平可能会缓冲久坐时间对大脑的负面影响。
