Aging is a fundamental biological process and age-related diseases have become the leading causes of death in modern societies. The objective of the Brown University Molecular Biology of Aging Predoctoral Graduate Training Program (MBoA) is to train the next generation of scientists to attack the immensely challenging yet important task of understanding and eventually manipulating human aging. In its first four years of operation the MBoA has brought together molecular biologists, computational and population biologists, and clinicians to provide instruction and training to graduate students in the molecular mechanisms of aging. The MBoA provides PhD candidates with a strong academic and experimental foundation in the current landscape of molecular aging research, and equips them with the skills to pursue a research career in this field. Our understanding of aging has reached a watershed in the past 10-15 years that was enabled by the increasing use of forward genetics in simple model systems. Fifteen faculty trainers from seven different departments and two established graduate programs have come together and comprise the MBoA Training Program. Their research interests span from insulin/IGF signaling, chromatin structure, cellular senescence, mitochondrial function and protein quality control to degenerative disorders of the nervous system, heart and cartilage. The experimental systems span from the nematode and Drosophila to mammalian models including the mouse and a variety of cell culture models. Continuing support is requested at the previous level for four trainees per year for a period of five years. The MBoA Training Program operates as a track under the auspices of two existing and well established programs at Brown University, the Molecular Biology, Cell Biology and Biochemistry Graduate Program (MCB), and the Graduate Program in Pathobiology. Candidates for support are drawn from talented students in the program, either in their first year based on academic excellence, or in subsequent years based on the caliber of their research, and are supported for a period of two years. The MCB and Pathobiology programs have different, but with respect to the biology of aging, very complementary and synergistic areas of activity: MCB has expertise in molecular biology and model organisms, and Pathobiology in mammalian and human physiology and pathology. The combination and integration of these approaches is the cornerstone of the philosophy of the MBoA. While research in invertebrate models informs us on the fundamental molecular mechanisms of aging, these principles have to be interpreted in terms of mammalian physiology and ultimately integrated with human pathology. Only an interdisciplinary approach can hope to implement therapies to alleviate the suffering caused by age-associated degenerative processes.
The increase of more than 25 years in the average life expectancy of Americans during the 20th century is remarkable. This rapid increase of our elderly population however has led to a burden of disease and disability that threatens to overwhelm our society. Fortunately, research is beginning to identify universal mechanisms that determine and even regulate the aging of all organisms, including humans, and impact all organ systems. The objective of this predoctoral training program is to train the next generation of scientists to engage in interdisciplinary research aimed at discovering and implementing therapies that alleviate the suffering caused by age-associated degenerative processes.
|Post, Stephanie; Karashchuk, Galina; Wade, John D et al. (2018) Drosophila Insulin-Like Peptides DILP2 and DILP5 Differentially Stimulate Cell Signaling and Glycogen Phosphorylase to Regulate Longevity. Front Endocrinol (Lausanne) 9:245|
|Behar, Joachim A; Rosenberg, Aviv A; Shemla, Ori et al. (2018) A Universal Scaling Relation for Defining Power Spectral Bands in Mammalian Heart Rate Variability Analysis. Front Physiol 9:1001|
|Adebayo Michael, Adeola O; Ahsan, Nagib; Zabala, Valerie et al. (2017) Proteomic analysis of laser capture microdissected focal lesions in a rat model of progenitor marker-positive hepatocellular carcinoma. Oncotarget 8:26041-26056|
|Lin, Feng; Hossain, Mohammed Akhter; Post, Stephanie et al. (2017) Total Solid-Phase Synthesis of Biologically Active Drosophila Insulin-Like Peptide 2 (DILP2). Aust J Chem 70:208-212|
|Morrissey, Patrick J; Murphy, Kevin R; Daley, Jean M et al. (2017) A novel method of standardized myocardial infarction in aged rabbits. Am J Physiol Heart Circ Physiol 312:H959-H967|
|Kim, Sun Y; Webb, Ashley E (2017) Neuronal functions of FOXO/DAF-16. Nutr Healthy Aging 4:113-126|
|Kang, Ping; Chang, Kai; Liu, Ying et al. (2017) Drosophila Kruppel homolog 1 represses lipolysis through interaction with dFOXO. Sci Rep 7:16369|
|Kaye, Emily G; Kurbidaeva, Amina; Wolle, Daniel et al. (2017) Drosophila Dosage Compensation Loci Associate with a Boundary-Forming Insulator Complex. Mol Cell Biol 37:|
|Jones, Brian C; Wood, Jason G; Chang, Chengyi et al. (2016) A somatic piRNA pathway in the Drosophila fat body ensures metabolic homeostasis and normal lifespan. Nat Commun 7:13856|
|Kuzu, Guray; Kaye, Emily G; Chery, Jessica et al. (2016) Expansion of GA Dinucleotide Repeats Increases the Density of CLAMP Binding Sites on the X-Chromosome to Promote Drosophila Dosage Compensation. PLoS Genet 12:e1006120|
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