Age is the largest single risk factor for the majority of diseases seen in clinics throughout the U.S. Demographic calculations predict that eliminating any single age-related disease would produce only a modest increase in human health span (years of healthy life) or life span. However, postponing or decreasing the rate of aging would retard the course of multiple age-related diseases and thus substantially increase health span and likely life span. Our ability to develop rational approaches to preventing or intervening in th debilitating and costly consequences of aging depends crucially on a thorough understanding of the causes of aging and how they interact with the etiology of specific age-related diseases. Training young scientists to integrate research on basic aging mechanisms with mechanisms of specific age-related diseases is a critical objective of this application. The long-term goal of ths training program is to provide exceptional young scientists with the broad knowledge, skills and interactions they will need to mitigate, through research, the enormous human and financial burdens caused by aging and age-related diseases. Each year, the program will train 12 talented postdoctoral scientists who will conduct research for a 2-year period in one or more of 32 laboratories headed by outstanding preceptors at the Buck Institute for Research on Aging, Lawrence Berkeley National Laboratory, University of California, Berkeley and Stanford University. Trainees will participate in research projects that include basic mechanisms of cellular stress responses, protein homeostasis, genomic and epigenomic stability, stem cell maintenance, bioenergetics and energy metabolism and hormonal, growth factor and nutrient signaling path- ways. They will utilize a variety of model systems including yeast, round and flat worms, fruit flies, fish, mice and human cells and tissues. And they will focus on an array of age-related diseases including Alzheimer's, Parkinson's and Huntington's diseases, stroke, cardiac and vascular dysfunction, cancer, diabetes, osteoporosis and sarcopenia. Trainees will be instructed in state-of-the-art techniques in genomics, epigenomics, drug screening, proteomics and metabolomics, as well as genetics, biochemistry, structural biology, cell biology, and cell and organismal imaging. They will receive the benefits of diverse seminar series and other scientific events and frequent networking opportunities. They will also attend courses in specialized scientific topics, as well as courses in ethics, presentation skills, proposal and manuscript writing, and laboratory management skills. The program will fill an important national and international need for high-quality advanced training that integrates basic aging research with research on age-related disease.
This postdoctoral training Program will prepare scientists from a range of disciplines for independent careers in research that aims to understand the mechanisms of aging and age-related disease. We will train the next generation of scientists and provide them with the broad knowledge, interdisciplinary skills and scientific interactions they will need to alleviate, through research, the enormous human and financial burdens caused by aging and age-related diseases.
|Wilson-Edell, Kathleen A; Yevtushenko, Mariya A; Rothschild, Daniel E et al. (2014) mTORC1/C2 and pan-HDAC inhibitors synergistically impair breast cancer growth by convergent AKT and polysome inhibiting mechanisms. Breast Cancer Res Treat 144:287-98|
|McCormick, Mark A; Mason, Amanda G; Guyenet, Stephan J et al. (2014) The SAGA histone deubiquitinase module controls yeast replicative lifespan via Sir2 interaction. Cell Rep 8:477-86|
|Shin, David S; Pratt, Ashley J; Tainer, John A (2014) Archaeal genome guardians give insights into eukaryotic DNA replication and damage response proteins. Archaea 2014:206735|
|Pratt, Ashley J; Shin, David S; Merz, Gregory E et al. (2014) Aggregation propensities of superoxide dismutase G93 hotspot mutants mirror ALS clinical phenotypes. Proc Natl Acad Sci U S A 111:E4568-76|
|Flynn, James M; O'Leary, Monique N; Zambataro, Christopher A et al. (2013) Late-life rapamycin treatment reverses age-related heart dysfunction. Aging Cell 12:851-62|
|Lee, Do Yup; Xun, Zhiyin; Platt, Virginia et al. (2013) Distinct pools of non-glycolytic substrates differentiate brain regions and prime region-specific responses of mitochondria. PLoS One 8:e68831|
|Lieu, Christopher A; Chinta, Shankar J; Rane, Anand et al. (2013) Age-related behavioral phenotype of an astrocytic monoamine oxidase-B transgenic mouse model of Parkinson's disease. PLoS One 8:e54200|
|Flynn, James M; Melov, Simon (2013) SOD2 in mitochondrial dysfunction and neurodegeneration. Free Radic Biol Med 62:4-12|
|Platt, Virginia; Lee, Do Yup; Canaria, Christie A et al. (2013) Towards understanding region-specificity of triplet repeat diseases: coupled immunohistology and mass spectrometry imaging. Methods Mol Biol 1010:213-30|
|Lucanic, Mark; Graham, Jill; Scott, Gary et al. (2013) Age-related micro-RNA abundance in individual C. elegans. Aging (Albany NY) 5:394-411|
Showing the most recent 10 out of 28 publications