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中文摘要
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描述(由申请者提供):2013年戈登衰老生物学研究会议(GRC)将是自1962年该系列成立以来的第29届。这一系列很重要,因为衰老的基础生物学研究在大型社会会议上的代表性很低,这些会议传统上主要强调老年学问题及其医学、社会和心理分支。因此,基础科学研究人员寻求将老龄化生物学全球研究中心作为讨论该领域最新进展、展示新的实验模型、范式的挑战、联网和启动合作项目的理想论坛。随着老龄化领域的成熟,S准备开始将生物学的各个领域整合到衰老的基础生物学中去,在模式生物中。随着年龄的增长,各种细胞过程和组织的动态平衡也变得越来越明显,这是衰老过程的原因。因此,2013年老龄化生物学全球研究报告将聚焦于“动态平衡与衰老”。该项目专注于细胞过程的动态平衡,包括生物钟、茎干、线粒体功能、脂肪代谢和蛋白质周转如何随着年龄的增长而下降,并导致衰老过程。此外,该会议旨在研究包括肌肉、脂肪、神经元和肠道在内的各种组织如何随着年龄的增长而衰退,并引起系统范围的扰动,从而导致有机体的全球衰退。所有这些都极大地扩展了老龄化研究的视野,并暗示了有可能提高健康寿命的干预措施的追求。虽然我们关于衰老生物学的大部分知识都来自于使用模型生物的研究,但最近,人类已经成为实验的对象,这些实验测试这些机制被保存得有多好,以及它们如何影响人类的衰老和与衰老相关的疾病。因此,这些不同领域的研究人员之间的相互反馈是2013年衰老生物学GRC的主要目标之一。为了实现这一目标,2013年老龄化生物学全球研究委员会将:1)促进对关键问题的公开讨论,特别强调可能对人类老龄化具有重要翻译潜力的新机制;2)提供一个论坛,讨论人类老龄化生物学研究的最新进展 其中包括:(1)促进老龄问题研究;3)促进思想交流和研究结果的沟通,以确定该领域未来的目标;4)促进联网、发起国际合作努力和联合体;以及5)促进初级研究人员融入既定的老龄研究人员群体。为实现这最后一个目标,将举办一次戈登-凯南研究研讨会,致力于培训学员的智力和心理准备,以便充分参与随后的全球资源中心。
英文摘要
DESCRIPTION (provided by applicant): The 2013 Gordon Research Conference (GRC) on Biology of Aging will be the twenty-ninth of its kind since inception of the series in 1962. This series is important because research in basic biology of aging has been poorly represented in the large society meetings that have traditionally maintained a major emphasis on gerontological issues and their medical, social, and psychological ramifications. Consequently, basic science investigators have sought the GRC on Biology of Aging as the ideal forum for discussion of recent advances in the field, presentation of new experimental models, challenge of paradigms, networking, and initiation of collaborative projects. As the aging field matures, it s ready to begin to integrate various areas of biology into the basic biology of aging in model organisms. It is also becoming apparent that homeostasis of various cellular processes and tissues declines with age which is causal to the aging process. Hence, the 2013 GRC on the Biology of Aging will focus on "homeostasis and aging." The program focuses on how homeostasis of cellular processes including circadian clocks, stemness, mitochondrial function, fat metabolism and protein turnover declines with age and is causal to the aging process. Furthermore, the conference aims to examine how various tissues including muscle, fat, neurons and gut decline with age and cause system wide perturbations that cause global decline of the organism. All of these greatly expand the horizons of aging research and suggest the pursuit of interventions that have the potential to enhance health span. While much of our knowledge about the biology of aging has derived from studies using model organisms, recently, humans have become the subjects of experiments that test how well these mechanisms are conserved and how they impact aging and age-related diseases in humans. Therefore, reciprocal feedback between investigators in these diverse fields is one of the main objectives of the 2013 Biology of Aging GRC. To accomplish this objective, the 2013 GRC on the Biology of Aging will: 1) promote open discussion of critical questions with particular emphasis on novel mechanisms that could have important translational potential for human aging; 2) provide a forum for the discussion of state-of-the art advances in research in biology of aging; 3) facilitate exchange of ideas and communication of findings that could shape the future goals of the field; 4) promote networking, initiation of international cooperative efforts, and consortiums; and, 5) promote the integration of junior investigators into the established community of aging researchers. This last objective will be met by inclusion of a Gordon-Kenan Research Seminar dedicated to the intellectual and psychological preparation of trainees for full participation in the GRC to follow.
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Targeting conserved diet-responsive transcriptional networks in neurons to slow neurodegeneration in Alzheimer's disease
Methylglyoxal drives astrocyte senescence to mediate neurodegeneration in Alzheimer's disease
Methylglyoxal drives astrocyte senescence to mediate neurodegeneration in Alzheimer's disease
Methylglyoxal drives astrocyte senescence to mediate neurodegeneration in Alzheimer's disease
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