Related Experiment Videos
Age-dependent impairment of mitochondrial function in primate brain
A C Bowling1, E M Mutisya, L C Walker
1Neurochemistry Laboratory, Massachusetts General Hospital, Boston 02114.
Journal of Neurochemistry
|May 1, 1993
Summary
Aging impairs brain function due to mitochondrial DNA damage. This study found age-related declines in mitochondrial complex I and IV activities in primate brains, supporting the oxidative stress hypothesis.
Area of Science:
- Neuroscience
- Gerontology
- Mitochondrial Biology
Background:
- Aging is linked to functional decline, potentially due to mitochondrial DNA oxidative damage.
- Oxidative damage to mitochondrial DNA can disrupt oxidative phosphorylation, affecting cellular energy production.
Purpose of the Study:
- To investigate the relationship between aging and the activity of enzymes involved in oxidative phosphorylation in primate cerebral cortex.
- To test the hypothesis that age-associated functional impairments stem from oxidative damage to mitochondrial DNA.
Main Methods:
- Assayed activities of mitochondrial complexes I, II-III, IV, and V, and citrate synthase in primate brain samples.
- Corrected enzyme activities for citrate synthase to account for mitochondrial enrichment.
- Used linear regression to analyze the correlation between enzyme activities and age.
Main Results:
- Significant negative correlations were found between age and the activities of mitochondrial complex I (p < 0.002) and complex IV (p < 0.03).
- Activities of complex I and IV showed progressive age-related reductions, even after correction for mitochondrial content.
- No significant changes in complex II-III or complex V activities were observed with age.
Conclusions:
- The study demonstrates an age-associated decline in mitochondrial complex I and complex IV activities in primate cerebral cortices.
- These findings support the role of oxidative damage to mitochondrial DNA in age-related functional impairments of the brain.