CADB Summer School 2004: Mitochondrial Disease and Aging

描述(由申请人提供)： 虽然线粒体基因组的突变在老年哺乳动物中更为普遍，但线粒体突变与衰老发病机制之间的关系尚不清楚。在神经细胞中，线粒体功能障碍、凋亡和坏死都可以追溯到线粒体对各种毒物的反应中钙的积累。这种钙的积累最初会促进能量代谢，但最终可能会损害ATP的产生，加速ROS的产生。线粒体蛋白(如细胞色素c，AIF)的释放容易通过caspase依赖和独立的途径触发细胞凋亡。这些蛋白质从膜间隙释放的机制仍然是细胞生物学中一个令人兴奋和有争议的方面。明确这些机制及其调控对于理解急性和慢性神经退行性疾病的发病机制至关重要。罗切斯特大学衰老和发育生物学中心发起了一项每年一度的暑期学校计划，面向15-20名神经科学家(高级研究生、博士后研究员，可能还有初级教员)。学生将在2003年下半年以竞争性方式选拔。将有10-15名特邀教员和几名来自罗切斯特大学的教员担任讲师。该大学最近在线粒体研究上投入了大量资金：招聘新教师，支持一系列座谈会，并开设线粒体生物学研究生课程。沿着这一思路，2004年首届计划的主题将是线粒体疾病和衰老。会议将于2004年8月6日至10日举行。选择这些日期是为了尽量减少与其他预定会议的冲突，并利用宿舍；住宿安排类似于类似的小型会议，并将促进学生和教职员工之间的社会和科学互动。

DESCRIPTION (provided by applicant): Although it is clear that mutations of the mitochondrial genome are more prevalent in aged mammals, the relationship between mitochondrial mutation and the pathogenesis of aging is poorly understood. In neuronal cells, mitochondrial dysfunction, apoptosis and necrosis can all be traced to mitochondrial calcium accumulation in response to a variety of toxicants. This calcium accumulation initially promotes energy metabolism but may ultimately impair ATP production and accelerate ROS production. The release of mitochondrial proteins (e.g., cytochrome c, AIF) can readily trigger apoptosis through caspase dependent and independent pathways. The mechanism by which these proteins are released from the intermembrane space remains an exciting and controversial aspect of cellular biology. Defining these mechanisms and their regulation will be critical in understanding the pathogenesis of both acute and chronic neurodegenerative diseases. The Center for Aging and Developmental Biology at the University of Rochester has initiated an annual summer school program for 15-20 neuroscientists (senior graduate students, postdoctoral fellows, and perhaps junior faculty). Students will be selected on a competitive basis in the second half of 2003. There would be 10-15 invited faculty members and several from the University of Rochester that will serve as instructors. The University has recently invested heavily in mitochondrial research: hiring new faculty, supporting a colloquium series, and creating a graduate course in mitochondrial biology. Along this vein, the theme for the inaugural program in 2004 will be Mitochondrial Disease and Aging. It will be held August 6 -10, 2004. These dates were chosen to minimize conflicts with other scheduled meetings and to take advantage of dormitory housing; the housing arrangement mirrors similar small conferences and will facilitate social and scientific interactions between students and faculty.