Project 458803

Aging is the greatest risk factor for age-related diseases such as cancer, diabetes, cardiovascular disease, and neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's disease. As an increasing number of Canadians are reaching advanced ages and are being impacted by these diseases, it is important to advance our understanding of the aging process, in order to promote healthy aging and limit age-related diseases. Studies have provided evidence indicating that mitochondria, the powerhouse within cells responsible for producing cellular energy, play a significant role in the aging process. Multiple mitochondria exist in the form of an interconnected network within a single cell, where they can undergo fission, to break away from this network, or fusion, to join this network. High mitochondrial network connectivity has been reported in healthy long-lived humans, while low mitochondrial network connectivity has been reported in cells from individuals with neurodegeneration. We and others have found that genetically altering mitochondrial dynamics (fission and fusion) can increase lifespan, enhance resistance to stress and can be protective in models of neurodegenerative diseases. Despite these exciting findings, little is known about how altering mitochondrial dynamics provides such beneficial effects. Thus, using C. elegans as a model organism to study aging, this work aims to determine the specific parameters and conditions required for altered mitochondrial dynamics to provide increased longevity. This work will therefore provide essential insight into the relationship between mitochondrial dynamics and longevity which can be useful in developing therapeutic targets to promote healthy aging and limit age-related diseases.