Hippocampal neurogenesis (HN) occurs throughout the life course and is important for memory and mood. Declining with age, HN plays a pivotal role in cognitive decline (CD), dementia, and late-life depression, such that altered HN could represent a neurobiological susceptibility to these conditions. Pertinently, dietary patterns (e.g., Mediterranean diet) and/or individual nutrients (e.g., vitamin D, omega 3) can modify HN, but also modify risk for CD, dementia, and depression. Therefore, the interaction between diet/nutrition and HN may alter risk trajectories for these ageing-related brain conditions. Using a subsample (n = 371) of the Three-City cohort—where older adults provided information on diet and blood biobanking at baseline and were assessed for CD, dementia, and depressive symptomatology across 12 years—we tested for interactions between food consumption, nutrient intake, and nutritional biomarker concentrations and neurogenesis-centred susceptibility status (defined by baseline readouts of hippocampal progenitor cell integrity, cell death, and differentiation) on CD, Alzheimer’s disease (AD), vascular and other dementias (VoD), and depressive symptomatology, using multivariable-adjusted logistic regression models. Increased plasma lycopene concentrations (OR [95% CI] = 1.07 [1.01, 1.14]), higher red meat (OR [95% CI] = 1.10 [1.03, 1.19]), and lower poultry consumption (OR [95% CI] = 0.93 [0.87, 0.99]) were associated with an increased risk for AD in individuals with a neurogenesis-centred susceptibility. Increased vitamin D consumption (OR [95% CI] = 1.05 [1.01, 1.11]) and plasma γ-tocopherol concentrations (OR [95% CI] = 1.08 [1.01, 1.18]) were associated with increased risk for VoD and depressive symptomatology, respectively, but only in susceptible individuals. This research highlights an important role for diet/nutrition in modifying dementia and depression risk in individuals with a neurogenesis-centred susceptibility.

中文翻译：

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根据以神经发生为中心的脑衰老生物易感性，饮食和营养因素与老年人认知能力下降、痴呆和抑郁症状之间的关联


海马神经发生（HN）发生在整个生命过程中，对记忆和情绪很重要。 HN 随着年龄的增长而下降，在认知能力下降 (CD)、痴呆和晚年抑郁症中发挥着关键作用，因此改变的 HN 可能代表对这些疾病的神经生物学易感性。相应地，饮食模式（例如地中海饮食）和/或个体营养素（例如维生素 D、omega 3）可以改变 HN，但也可以改变 CD、痴呆和抑郁症的风险。因此，饮食/营养与 HN 之间的相互作用可能会改变这些与衰老相关的大脑疾病的风险轨迹。使用三城市队列的子样本 (n = 371)（其中老年人在基线时提供有关饮食和血液生物库的信息，并评估 12 年来的 CD、痴呆和抑郁症状），我们测试了食物消耗、 CD、阿尔茨海默病 (AD)、血管性和其他痴呆 (VoD) 以及抑郁症状的营养摄入量、营养生物标志物浓度以及以神经发生为中心的易感性状态（由海马祖细胞完整性、细胞死亡和分化的基线读数定义） ，使用多变量调整逻辑回归模型。血浆番茄红素浓度升高（OR [95% CI] = 1.07 [1.01, 1.14]），红肉摄入量增加（OR [95% CI] = 1.10 [1.03, 1.19]），家禽摄入量降低（OR [95% CI]） = 0.93 [0.87, 0.99]）与具有以神经发生为中心的易感性的个体患 AD 的风险增加相关。维生素 D 消耗量增加（OR [95% CI] = 1.05 [1.01, 1.11]）和血浆 γ-生育酚浓度增加（OR [95% CI] = 1.08 [1.01, 1.18]）分别与 VoD 和抑郁症状风险增加相关，但仅限于易感个体。这项研究强调了饮食/营养在改变以神经发生为中心的易感性个体的痴呆和抑郁风险方面的重要作用。