Abstract

This proposal aims to investigate the origin and mechanism of accumulation of mitochondrial DNA damage in human tissues during aging. In one case a specific mitochondrial DNA deletion previously found only in patients affected with certain rare neuromuscular diseases but recently discovered in hearts and brains of normal aged individuals will be studied. The goal of this research is to determine the rate these deletions accumulate and why they accumulate to different levels in different brain regions in aged individuals. These studies may provide information on the origin of mitochondrial mutations and their contributions to aging.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
5R01AG011492-02
Application #
2052682
Study Section
Mammalian Genetics Study Section (MGN)
Project Start
1993-05-01
Project End
1996-04-30
Budget Start
1994-05-01
Budget End
1995-04-30
Support Year
2
Fiscal Year
1994
Total Cost
Indirect Cost

  Institution

Name
University of Southern California
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
041544081
City
Los Angeles
State
CA
Country
United States
Zip Code
90089

  Publications

Vitaterna, Martha Hotz; Ko, Caroline H; Chang, Anne-Marie et al. (2006) The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Proc Natl Acad Sci U S A 103:9327-32
Soong, N W; Dang, M H; Hinton, D R et al. (1996) Mitochondrial DNA deletions are rare in the free radical-rich retinal environment. Neurobiol Aging 17:827-31