The goal of this T32 program is to train new independent investigators who will utilize contemporary genetic and molecular genetic techniques to investigate the underlying mechanisms of aging. The rationale for the focus of our program can be succinctly summarized as follows: 1) The genetic approach to the analysis of the biology and pathobiology of aging has special merit that, by definition, it deals with primary, constitutional, heritable, controls of gene action and thus can inform us as to fundamental mechanisms. 2) The tools for the molecular genetic approach to the pathobiology of aging are becoming increasingly rich and diverse. We thus believe that this focus for gerontological research will be applied with increasing frequency and success. While this may seem obvious given today's prominence of molecular genetics, until recently the field of gerontology did not have so rich a historical background in use of genetic approaches. Thus, we believe there is a need for more investigators who are trained in the principles and methods of genetic analysis and in gerontology. Such training is the primary goal of this program. The program currently supports 8 pre- and 8 post-doctoral trainees, and we request to sustain these numbers. We provide continuity of training by typically providing support for 3-4 (pre-doc) or 2-3 (post-doc) years. Predoctoral candidates ordinarily begin in their 2nd year of graduate training and post-docs in their 1st year of post-graduate training. The relevance of this program to public health is rooted in fact that age is the primary risk factor for disease in our population: diseases associated with aging are the chief health burden to our society and the primary cause of reduced quality of life. An increased understanding of the genetic mechanisms responsible for the processes that contribute to the burden of disease in aging can have a great positive impact on our society. We are training bright, new scientists who are highly motivated to work to increase this understanding.

Public Health Relevance

The goal of this T32 program is to train new independent investigators who will utilize contemporary genetic and molecular genetic techniques to investigate the underlying mechanisms of aging. An increased understanding of the genetic mechanisms responsible for the processes that contribute to the burden of disease in aging can have a great positive impact on our society and we are training bright, new scientists who are highly motivated to work to increase this understanding.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Institutional National Research Service Award (T32)
Project #
5T32AG000057-37
Application #
8667371
Study Section
Special Emphasis Panel (ZAG1)
Program Officer
Velazquez, Jose M
Project Start
1978-07-01
Project End
2018-04-30
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
37
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Washington
Department
Pathology
Type
Schools of Medicine
DUNS #
City
Seattle
State
WA
Country
United States
Zip Code
98195
Bitto, Alessandro; Ito, Takashi K; Pineda, Victor V et al. (2016) Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice. Elife 5:
Ieronimakis, Nicholas; Hays, Aislinn; Prasad, Amalthiya et al. (2016) PDGFRα signalling promotes fibrogenic responses in collagen-producing cells in Duchenne muscular dystrophy. J Pathol 240:410-424
Chiao, Ying Ann; Kolwicz, Stephen C; Basisty, Nathan et al. (2016) Rapamycin transiently induces mitochondrial remodeling to reprogram energy metabolism in old hearts. Aging (Albany NY) 8:314-27
Campbell, Matthew D; Marcinek, David J (2016) Evaluation of in vivo mitochondrial bioenergetics in skeletal muscle using NMR and optical methods. Biochim Biophys Acta 1862:716-24
Hoekstra, Jake G; Hipp, Michael J; Montine, Thomas J et al. (2016) Mitochondrial DNA mutations increase in early stage Alzheimer disease and are inconsistent with oxidative damage. Ann Neurol 80:301-6
Davis, Marie Y; Trinh, Kien; Thomas, Ruth E et al. (2016) Glucocerebrosidase Deficiency in Drosophila Results in α-Synuclein-Independent Protein Aggregation and Neurodegeneration. PLoS Genet 12:e1005944
Davis, Marie Y; Johnson, Catherine O; Leverenz, James B et al. (2016) Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease. JAMA Neurol 73:1217-1224
Liu, Sophia Z; Marcinek, David J (2016) Skeletal muscle bioenergetics in aging and heart failure. Heart Fail Rev :
Tryon, Valerie L; Mizumori, Sheri J Y; Morgan, Michael M (2016) Analysis of morphine-induced changes in the activity of periaqueductal gray neurons in the intact rat. Neuroscience 335:1-8
Phelps, Michael; Stuelsatz, Pascal; Yablonka-Reuveni, Zipora (2016) Expression profile and overexpression outcome indicate a role for βKlotho in skeletal muscle fibro/adipogenesis. FEBS J 283:1653-68

Showing the most recent 10 out of 173 publications