2007 Aging, Biology of Gordon Conference

描述(申请者提供)：申请资助戈登衰老生物学研究会议(GRC)的部分资金。2007年会议的主题是“在老龄化过程中保持大分子完整性”，会议将于2007年9月23日至28日在瑞士Les Diablerets的Les Diablerets会议中心举行。拉多拉·V·汤普森博士、霍莉·布朗-博格博士和亚历山大·伯克尔博士将组织这项科学计划。我们在这里的目的是提供资金，支持受邀的演讲者、讨论领导者和初级科学家(博士后研究员、高级研究生或新的初级教员)，他们将从会议中受益并为会议做出贡献。我们邀请的演讲者在衰老的分子和细胞生物学、衰老生理学和衰老遗传学方面的研究在国际上都是公认的。众所周知，这些演讲者是他们的科学的强有力的传播者，他们激发并参与活跃的讨论。长期以来，DNA累积损伤一直被认为是导致衰老过程的主要损伤形式之一，哺乳动物的寿命与细胞DNA修复能力呈正相关。但已知的其他生物大分子，如蛋白质和脂类，也会经历分子损伤、聚集和错误折叠，这可能会导致衰老过程。干细胞和核受体目前正在深入研究它们在衰老过程中的作用。近年来，大量的遗传、药物和饮食干预措施被描述为在从单细胞生物体到人类的各种系统中延缓衰老。许多这类干预措施与细胞维持功能和/或细胞抗应激能力有机械联系；它们有望减少细胞和组织的脆弱性，从而防止与年龄有关的病理变化。最后，加速衰老的模型提高了我们对细胞维护和抗应激能力的理解。戈登研究会议将聚焦于这些热门话题。选择这些主题背后的理由是，模型系统调查细胞维护和完整性的结果显著收敛。会议的目标是：--批判性地评估衰老生物学方面的进展；确定衰老生物学是否能揭示与年龄相关的衰退和疾病的性质/原因；强调综合性和转化性的研究结果，以此作为一种手段，为延长健康寿命的治疗选择开发新的未来途径。戈登老龄化生物学研究会议的总体目的是将不同老龄化领域的研究人员和领域外的研究人员聚集在一起，讨论该领域的当前研究，并考虑将科学进步转化为临床干预措施的潜力。细胞大分子(如DNA、蛋白质、脂类)利用各种细胞过程(如修复、降解和替换)和几个模型系统(线虫、啮齿动物、真菌、加速衰老模型)保持完整性的能力，是衰老生物学和延长健康寿命的前沿。我们充分预计，这一领域的进展将为老年人的干预和生活质量铺平道路。

DESCRIPTION (provided by applicant): Funds are requested to provide partial support for the Gordon Research Conference (GRC) on the Biology of Aging. The theme of the 2007 conference will be "Maintenance of Macromolecular Integrity in Aging" to be held at the Les Diablerets Conference Center, Les Diablerets, Switzerland, from September 23 - 28, 2007. Drs. LaDora V. Thompson, Holly Brown-Borg and Alexander B¿rkle will organize the scientific program. Our aim here is to provide funds to support invited speakers, discussion leaders, and junior scientists (postdoctoral fellows, advanced graduate students, or new, junior faculty) who would benefit from and contribute to the conference. The speakers we have invited are internationally recognized for their research on the molecular and cellular biology of aging, physiology of aging, and genetics of aging. These speakers are known to be strong communicators of their science, who stimulate, and participate in, lively discussion. Accumulating damage of DNA has long been suggested as one of the major forms of damage that contribute to the aging process, and life spans of mammalian species positively correlate with the cellular capacity for DNA repair. But other biological macromolecules such as proteins and lipids are also known to undergo molecular damage, aggregation, and misfolding which could contribute to the aging process. Stem cells and nuclear receptors are currently being intensively investigated in their contribution to the aging process. In recent years, a large number of genetic, pharmacological and dietary interventions have been described that slow down aging in various systems ranging from unicellular organisms to humans. Many such interventions have been mechanistically linked with cellular maintenance functions and/or cellular stress resistance; they can be expected to reduce the vulnerability of cells and tissues and thus prevent age-related pathological changes. Lastly, models of accelerated aging have enhanced our understanding of cellular maintenance and stress resistance. The Gordon Research Conference will focus on these hot topics. The rationale behind the choice of these themes is the remarkable convergence of the results from the models systems to investigate cellular maintenance and integrity. The goals of the conference:-To critically assess progress in the biology of aging; To determine whether the biology of aging informs on the nature/causes of age-related decline and disease; To emphasize integrative and translational research findings as a means to develop novel future avenues for therapeutic options that extend health span. The overall purpose of the Gordon Research Conference on The Biology of Aging, "Maintenance of Macromolecular Integrity in Aging" is to bring together investigators in diverse areas of aging and investigators outside the field to discuss the current research in the field and to consider the potential to translate scientific progress into clinical interventions. The ability of cellular macromolecules (e.g., DNA, proteins, lipids) to maintain integrity, using various cellular processes (e.g. repair, degradation and replacement) and several model systems (C. elegans, rodents, fungal, accelerated aging models), is at the forefront of the biology of aging and the extension of health span. We fully anticipate that progress in this field will pave the way for interventions and quality of life for the older adult.