Mediterranean Diet, Alzheimer Disease Biomarkers, and Brain Atrophy in Old Age
Mediterranean Diet, Alzheimer Disease Biomarkers, and Brain Atrophy in Old Age
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DOI：
10.1212/wnl.0000000000012067
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发表时间：
2021-06-15
期刊：
影响因子：
9.9
通讯作者：
Wagner, Michael
中科院分区：
文献类型：
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作者：
Ballarini, Tommaso;van Lent, Debora Melo;Wagner, Michael
目的为了确定遵循地中海式饮食(MEDI)是否与阿尔茨海默病(AD)的认知功能和体内生物标志物有关，我们分析了德国DZNE-纵向认知障碍和痴呆研究的横断面数据。方法样本512例，平均年龄69.5±-5.9岁，包括169例认知正常的受试者和AD高危个体(其中53例为AD亲属，209例为主观认知功能减退，81例为轻度认知功能障碍)。我们根据食物频率问卷来定义MEDI依从性。通过T1-MRI上基于体素的形态测量产生脑体积结果，并使用广泛的神经心理学组件评估认知能力。对226例受试者进行脑脊液中AD相关生物标志物(β-淀粉样蛋白(42/40)[Aβ(42/40)]比值、磷酸化tau181[pTau181])的检测。我们通过控制几个协变量的线性回归模型分析了MEDI和预后之间的关系。此外，我们还使用了假设驱动的中介和调节分析。结果较高的中膜粘附性与较大的内侧灰质体积(P<；0.05家族性误差校正)、较好的记忆力(β+/-SE=0.03+/-0.02；p=0.038)、较少的淀粉样蛋白(Aβ(42/40)比率，β+/-SE=0.003+/-0.001；p=0.008)和pTau181(β+/-SE=-1.96+/-0.68；p=0.004)病理改变有关。中时容量在MEDI与记忆的联系中起中介作用(40%的间接中介作用)。最后，MEDI有利地缓和了Aβ(42/40)比率、pTau181和内侧颞叶萎缩之间的联系。结果与APOE-epsilon 4状态的纠正一致。结论我们的研究结果证实了MEDI是防止记忆衰退和内侧颞叶萎缩的保护性因素的观点。他们认为，这些联系可能由淀粉样变性和tau病理的减少来解释。纵向和饮食干预研究应进一步检验这一猜想及其治疗意义。
Objective To determine whether following a Mediterranean-like diet (MeDi) relates to cognitive functions and in vivo biomarkers for Alzheimer disease (AD), we analyzed cross-sectional data from the German DZNE-Longitudinal Cognitive Impairment and Dementia Study. Method The sample (n = 512, mean age 69.5 +/- 5.9 years) included 169 cognitively normal participants and individuals at higher AD risk (53 with relatives with AD, 209 with subjective cognitive decline, and 81 with mild cognitive impairment). We defined MeDi adherence according to the food frequency questionnaire. Brain volume outcomes were generated via voxel-based morphometry on T1-MRI, and cognitive performance was assessed with an extensive neuropsychological battery. AD-related biomarkers (beta-amyloid(42/40) [A beta(42/40)] ratio, phosphorylated tau 181 [pTau181]) in CSF were assessed in n = 226 individuals. We analyzed the associations between MeDi and outcomes with linear regression models controlling for several covariates. In addition, we applied hypothesis-driven mediation and moderation analysis. Results Higher MeDi adherence related to larger mediotemporal gray matter volume (p < 0.05 family-wise error corrected), better memory (beta +/- SE = 0.03 +/- 0.02; p = 0.038), and less amyloid (A beta(42/40) ratio, beta +/- SE = 0.003 +/- 0.001; p = 0.008) and pTau181 (beta +/- SE = -1.96 +/- 0.68; p = 0.004) pathology. Mediotemporal volume mediated the association between MeDi and memory (40% indirect mediation). Finally, MeDi favorably moderated the associations among A beta(42/40) ratio, pTau181, and mediotemporal atrophy. Results were consistent correcting for APOE-epsilon 4 status. Conclusion Our findings corroborate the view of MeDi as a protective factor against memory decline and mediotemporal atrophy. They suggest that these associations might be explained by a decrease of amyloidosis and tau pathology. Longitudinal and dietary intervention studies should further examine this conjecture and its treatment implications.