Coffee polyphenols ameliorate early-life stress-induced cognitive deficits in male mice

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress Pub Date : 2024-05-15 DOI:10.1016/j.ynstr.2024.100641

J. Geertsema , M. Kratochvil , R. González-Domínguez , S. Lefèvre-Arbogast , D.Y. Low , A. Du Preez , H. Lee , M. Urpi-Sarda , A. Sánchez-Pla , L. Aigner , C. Samieri , C. Andres-Lacueva , C. Manach , S. Thuret , P.J. Lucassen , A. Korosi

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引用次数: 0

Abstract

Stress exposure during the sensitive period of early development has been shown to program the brain and increases the risk to develop cognitive deficits later in life. We have shown earlier that early-life stress (ES) leads to cognitive decline at an adult age, associated with changes in adult hippocampal neurogenesis and neuroinflammation. In particular, ES has been shown to affect neurogenesis rate and the survival of newborn cells later in life as well as microglia, modulating their response to immune or metabolic challenges later in life. Both of these processes possibly contribute to the ES-induced cognitive deficits. Emerging evidence by us and others indicates that early nutritional interventions can protect against these ES-induced effects through nutritional programming. Based on human metabolomics studies, we identified various coffee-related metabolites to be part of a protective molecular signature against cognitive decline in humans. Caffeic and chlorogenic acids are coffee-polyphenols and have been described to have potent anti-oxidant and anti-inflammatory actions. Therefore, we here aimed to test whether supplementing caffeic and chlorogenic acids to the early diet could also protect against ES-induced cognitive deficits. We induced ES via the limited nesting and bedding paradigm in mice from postnatal(P) day 2–9. On P2, mice received a diet to which 0.02% chlorogenic acid (5-O-caffeoylquinic acid) + 0.02% caffeic acid (3′,4′-dihydroxycinnamic acid) were added, or a control diet up until P42. At 4 months of age, all mice were subjected to a behavioral test battery and their brains were stained for markers for microglia and neurogenesis. We found that coffee polyphenols supplemented early in life protected against ES-induced cognitive deficits, potentially this is mediated by the survival of neurons or microglia, but possibly other mechanisms not studied here are mediating the effects. This study provides additional support for the potential of early nutritional interventions and highlights polyphenols as nutrients that can protect against cognitive decline, in particular for vulnerable populations exposed to ES.

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咖啡多酚可改善雄性小鼠早期生活压力引起的认知缺陷

事实证明，在早期发育的敏感时期受到的压力会对大脑产生影响，并增加日后出现认知障碍的风险。我们早些时候已经证明，早期生活压力（ES）会导致成年后的认知能力下降，这与成年海马神经发生和神经炎症的变化有关。特别是，ES 已被证明会影响神经发生率和新生细胞的存活率，并影响小胶质细胞，从而调节它们对免疫或新陈代谢挑战的反应。这两个过程都可能导致 ES 引起的认知障碍。我们和其他研究人员的新证据表明，早期营养干预可以通过营养编程防止 ES 诱导的这些影响。基于人类代谢组学研究，我们发现与咖啡有关的各种代谢物是防止人类认知能力下降的保护性分子特征的一部分。咖啡酸和绿原酸是咖啡多酚，据描述具有强大的抗氧化和抗炎作用。因此，我们在此旨在测试在早期饮食中补充咖啡酸和绿原酸是否也能保护ES诱导的认知缺陷。我们在小鼠出生后（P）第 2-9 天通过有限嵌套和铺垫范例诱导 ES。小鼠在出生后第2天开始摄入添加0.02%绿原酸（5-O-咖啡酰奎宁酸）+0.02%咖啡酸（3′,4′-二羟基肉桂酸）的食物，或在出生后第42天之前摄入对照食物。在小鼠 4 个月大时，对所有小鼠进行行为测试，并对其大脑进行染色，以检测小胶质细胞和神经发生的标记物。我们发现，在小鼠生命早期补充咖啡多酚可以防止 ES 诱导的认知缺陷，这可能是通过神经元或小胶质细胞的存活来实现的，但也可能是其他未研究的机制在起作用。这项研究为早期营养干预的潜力提供了更多支持，并强调了多酚类物质是可以防止认知能力下降的营养物质，尤其是对于暴露于 ES 的脆弱人群。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neurobiology of Stress Biochemistry, Genetics and Molecular Biology-Biochemistry

CiteScore

9.40

自引率

4.00%

发文量

审稿时长

48 days

期刊介绍： Neurobiology of Stress is a multidisciplinary journal for the publication of original research and review articles on basic, translational and clinical research into stress and related disorders. It will focus on the impact of stress on the brain from cellular to behavioral functions and stress-related neuropsychiatric disorders (such as depression, trauma and anxiety). The translation of basic research findings into real-world applications will be a key aim of the journal. Basic, translational and clinical research on the following topics as they relate to stress will be covered: Molecular substrates and cell signaling, Genetics and epigenetics, Stress circuitry, Structural and physiological plasticity, Developmental Aspects, Laboratory models of stress, Neuroinflammation and pathology, Memory and Cognition, Motivational Processes, Fear and Anxiety, Stress-related neuropsychiatric disorders (including depression, PTSD, substance abuse), Neuropsychopharmacology.