ObjectivePeople who eat healthier diets are less likely to develop dementia, but the biological mechanism of this protection is not well understood. We tested the hypothesis that healthy diet protects against dementia because it slows the pace of biological aging.MethodsWe analyzed Framingham Offspring Cohort data. We included participants ≥60 years‐old, free of dementia and having dietary, epigenetic, and follow‐up data. We assessed healthy diet as long‐term adherence to the Mediterranean‐Dash Intervention for Neurodegenerative Delay diet (MIND, over 4 visits spanning 1991–2008). We measured the pace of aging from blood DNA methylation data collected in 2005–2008 using the DunedinPACE epigenetic clock. Incident dementia and mortality were defined using study records compiled from 2005 to 2008 visit through 2018.ResultsOf n = 1,644 included participants (mean age 69.6, 54% female), n = 140 developed dementia and n = 471 died over 14 years of follow‐up. Greater MIND score was associated with slower DunedinPACE and reduced risks for dementia and mortality. Slower DunedinPACE was associated with reduced risks for dementia and mortality. In mediation analysis, slower DunedinPACE accounted for 27% of the diet‐dementia association and 57% of the diet‐mortality association.InterpretationFindings suggest that slower pace of aging mediates part of the relationship of healthy diet with reduced dementia risk. Monitoring pace of aging may inform dementia prevention. However, a large fraction of the diet‐dementia association remains unexplained and may reflect direct connections between diet and brain aging that do not overlap other organ systems. Investigation of brain‐specific mechanisms in well‐designed mediation studies is warranted. ANN NEUROL 2024

中文翻译：

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弗雷明汉心脏研究中的饮食、生物衰老速度和痴呆风险

目的饮食健康的人患痴呆症的可能性较小，但这种保护的生物学机制尚不清楚。我们测试了健康饮食可以预防痴呆症的假设，因为它可以减缓生物衰老的速度。方法我们分析了弗雷明汉后代队列数据。我们纳入了 60 岁以上、无痴呆症且有饮食、表观遗传和随访数据的参与者。我们将健康饮食评估为长期坚持地中海-Dash 神经退行性延迟干预饮食（MIND，1991 年至 2008 年期间超过 4 次就诊）。我们使用 DunedinPACE 表观遗传时钟，根据 2005 年至 2008 年收集的血液 DNA 甲基化数据测量了衰老速度。痴呆症事件和死亡率是使用 2005 年至 2008 年访问至 2018 年期间编制的研究记录来定义的。结果 n = 1,644 名参与者（平均年龄 69.6 岁，54% 为女性），n = 140 人患上痴呆症，n = 471 人在 14 年的随访中死亡。向上。MIND 得分越高，达尼丁 PACE 速度越慢，痴呆和死亡风险降低。但尼丁PACE 速度较慢与痴呆和死亡风险降低相关。在中介分析中，较慢的 DunedinPACE 占饮食与痴呆关联的 27%，占饮食与死亡率关联的 57%。 研究结果表明，衰老速度较慢在一定程度上介导了健康饮食与痴呆风险降低之间的关系。监测衰老速度可以为痴呆症的预防提供信息。然而，饮食与痴呆之间的很大一部分关联仍然无法解释，可能反映了饮食与大脑衰老之间的直接联系，并且与其他器官系统没有重叠。有必要在精心设计的中介研究中研究大脑特异性机制。安神经学 2024