Interactions between diet and cognition

饮食与认知之间的相互作用

基本信息

批准号：
10215502
负责人：
Scott Edward Kanoski
金额：
$ 42.93万
依托单位：
UNIVERSITY OF SOUTHERN CALIFORNIA
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-09-20 至 2023-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10215502
关键词：
Adolescence Adolescent Adult Anatomy Attenuated Behavioral Brain Brain region Carbohydrates Cells Child Cognition Consumption Cues Data Deoxyuridine Desire for food Development Diet Dietary Factors Dietary Fats Dietary Sugars Eating Energy Intake Exercise Feeding behaviors Female Fluorescent in Situ Hybridization Food Functional disorder Hippocampus (Brain)Human Immunohistochemistry Impaired cognition Impairment Intake Intervention Life Linear Regressions Link Memory Memory impairment Metabolic Metabolic dysfunction Mitotic Modeling Neurocognitive Deficit Neurons Obesity Obesity Epidemic Outcome Pathologic Performance Phase Population Process Public Health Publishing Rattus Rewards Role Running Saturated Fatty Acids Specificity Time Transplantation United States Weaning Weight Gain age group base cell type cognitive function cognitive process diet-induced obesity emerging adult energy balance experimental study feeding gut microbiome gut microbiota insight male memory process microbial microbiota transplantation negative affect neurobiological mechanism neurogenesis neuroinflammation obesogenic prevent social spatial memory sugar sweetened beverage treadmill

项目摘要

7. Project Summary: Dietary sugar consumption has dramatically risen in the U.S. over the past 60 years 1. In addition to being associated with body weight gain and harmful metabolic outcomes 2-7, emerging evidence reveals that excessive consumption of sugar and other “obesogenic” dietary factors (e.g., saturated fatty acids) negatively impacts memory function and other cognitive processes 8,9. Particularly concerning is the rise in sugar consumption among children, who with ~15-20% of their total daily caloric intake from added sugars (predominantly from sugar-sweetened beverages, SSBs) 10,11, are the highest sugar consumers of any age group. The juvenile and adolescent developmental phases are highly susceptible periods for the onset of metabolic dysfunction resulting from excessive sugar intake 6 and new evidence suggests that this period of development is also a particularly vulnerable time for sugar-related neurocognitive deficits 12,13. Therefore, it is important to understand the precise developmental periods and domains of cognition that are vulnerable to excessive consumption of added sugars during early life periods. Our preliminary data presented herein reveals that excessive consumption of SSBs (11% carbohydrate solution to match commonly consumed SSBs in the U.S.) in rats beginning at the onset of the juvenile period of development but not beginning during early adulthood impairs spatial memory function and increases neuroinflammation in the hippocampus 14, a brain region classically associated with spatial and declarative memory function and more recently with learned aspects of food intake control 15,16. Other preliminary data presented in this proposal offer insight into possible mechanisms linking early life sugar consumption with hippocampal-dependent memory impairments, as early life SSB access profoundly alters the gut microbiome and reduces markers of neurogenesis in the hippocampus. Proposed experiments will provide mechanistic insight into the relationship between early life sugar consumption and memory impairment by illuminating [1] the precise developmental periods and feeding- relevant memory processes that are particularly vulnerable to early life sugar consumption, [2] the underlying neurobiological mechanisms through which dietary factors during development influence cognition, and [3] intervention strategies that can potentially reverse the long-lasting memory deficits associated with excessive early life sugar consumption. Results will contribute toward understanding the underlying mechanisms through which obesogenic dietary factors influence cognition and may provide valuable insight toward reversing or preventing the pathological effects of unhealthy dietary factors on the brain.

7。项目摘要：在过去60年中，美国的饮食含糖量急剧上升1。除了体重增加和有害代谢结果2-7之外，新出现的证据揭示了糖和其他“肥胖”饮食因素的过量消耗（例如饱和脂肪酸）负面影响记忆功能和其他认知过程8,9。特别令人担忧的是上升儿童的糖消耗，他们的每日热量摄入量的约15-20％（主要来自糖含糖的卧室，SSB）10,11是任何年龄段的糖消费者最高的。少年和青少年的发育阶段是代谢发作的高度易感时期过量糖摄入6和新证据引起的功能障碍表明这一发展时期对于糖有关的神经认知，这也是一个特别脆弱的时间，定义了12,13。因此，重要的是了解容易受到过多的认知的确切发育时期和领域早期生命周期中添加的糖的消费。我们在此提供的初步数据表明 SSB的过量消费（11％的碳水解溶液匹配美国常见的SSB）大鼠从少年发育时期开始，但不是在成年初期开始损害空间记忆函数并增加海马区域的神经炎症，一个大脑区域与空间和声明性记忆功能相关联，最近与食物摄入控制15,16。本提案中介绍的其他初步数据提供了有关可能的洞察力尽早将早期糖消耗与海马依赖性记忆障碍联系起来的机制 Life SSB可以深刻地改变肠道微生物组，并减少海马中神经发生的标记。拟议的实验将提供有关早期糖之间关系的机械洞察力通过照明[1]精确的发育时期和喂养来消费和记忆障碍相关的记忆过程特别容易受到早期糖消费的影响，[2]基础神经生物学机制通过其在发育过程中影响认知的饮食因素，[3] 干预策略可能会扭转与多余的持久记忆相关的持久记忆早期糖消耗。结果将有助于理解基本机制肥胖的饮食因素会影响认知，并可以为您提供宝贵的见解逆转或防止不健康饮食因素对大脑的病理影响。