ANU College of Engineering & Computer Science, The Australian National University, Canberra, Australia.
Centre for Healthy Brain Ageing, Neuropsychiatric Institute, University of New South Wales, Sydney, Australia.
Int J Obes (Lond). 2018 Mar;42(3):455-461. doi: 10.1038/ijo.2017.254. Epub 2017 Oct 10.
High BMI at midlife is associated with increased risk of dementia as well as faster decline in cognitive function. In late-life, however, high BMI has been found to be associated with both increased and decreased dementia risk. The objective of this study was to investigate the neural substrates of this age-related change in body mass index (BMI) risk.
We measured longitudinal cortical thinning over the whole brain, based on magnetic resonance imaging scans for 910 individuals aged 44-66 years at baseline. Subjects were sampled from a large population study (PATH, Personality and Total Health through Life). After attrition and exclusions, the final analysis was based on 792 individuals, including 387 individuals aged 60-66 years and 405 individuals aged 44-49 years. A mixed-effects model was used to test the association between cortical thinning and baseline BMI, as well as percentage change in BMI.
Increasing BMI was associated with increased cortical thinning in posterior cingulate at midlife (0.014 mm kg m, confidence interval; CI=0.005, 0.023, P<0.05 false discovery rate (FDR) corrected). In late-life, increasing BMI was associated with reduced cortical thickness, most prominently in the right supramarginal cortex (0.010 mm kg m, CI=0.005-0.016, P<0.05 FDR corrected), as well as frontal regions. In late-life, decreasing BMI was also associated with increased cortical thinning, including right caudal middle frontal cortex (0.014 mm kg m (CI=0.006-0.023, P<0.05 FDR corrected).
The pattern of cortical thinning-in association with increasing BMI at both midlife and late-life-is consistent with known obesity-related dementia risk. Increased cortical thinning in association with decreasing BMI at late-life may help explain the 'obesity paradox', where high BMI in midlife appears to be a risk factor for dementia, but high BMI in late-life appears, at times, to be protective.
中年时期较高的 BMI 与痴呆风险增加以及认知功能下降速度加快有关。然而，在晚年，较高的 BMI 与痴呆风险的增加和降低都有关。本研究的目的是探讨与 BMI 风险相关的这种与年龄相关的变化的神经基础。
我们基于基线时对 910 名年龄在 44-66 岁的个体的磁共振成像扫描，测量了整个大脑的纵向皮质变薄。受试者是从一项大型人群研究（PATH，人格与终生健康）中抽样的。经过损耗和排除后，最终分析基于 792 名个体，包括 387 名 60-66 岁的个体和 405 名 44-49 岁的个体。使用混合效应模型来测试皮质变薄与基线 BMI 以及 BMI 变化百分比之间的关联。
BMI 增加与中年时后扣带回的皮质变薄增加有关（0.014 mm kg m，置信区间；CI=0.005，0.023，P<0.05 假发现率（FDR）校正）。在晚年，BMI 增加与皮质厚度减少有关，最明显的是右侧缘上回（0.010 mm kg m，CI=0.005-0.016，P<0.05 FDR 校正），以及额叶区域。在晚年，BMI 减少也与皮质变薄增加有关，包括右侧额中回后部（0.014 mm kg m（CI=0.006-0.023，P<0.05 FDR 校正）。
与中年和晚年 BMI 增加相关的皮质变薄模式与已知的肥胖相关痴呆风险一致。与晚年 BMI 减少相关的皮质变薄增加可能有助于解释“肥胖悖论”，即中年时期较高的 BMI 似乎是痴呆的一个危险因素，但晚年时期较高的 BMI 有时似乎具有保护作用。
