Judd Aiken
Judd Aiken is Professor at University of Alberta. Judd works on Biology and Etiology of Prions, and Mitochondrial DNA (mtDNA) mutations with special emphasis on mitochondrial aging. His research is conducted on mice and rhesus monkeys.
The loss of muscle mass and function with age is an inevitable component of the aging process. In humans, skeletal muscle fiber number in quadriceps declines from 600,000 at 50 years of age to 323,000 at 80 years. Judd's lab has shown that one cause of this decline in fiber number is the accumulation of mtDNA genomes containing large deletion mutations, and their studies suggest a progression of events beginning with the generation and accumulation of a mtDNA deletion mutation, the concomitant development of electron transport chain, a subsequent triggering of apoptotic and necrotic events, a process resulting in muscle fiber atrophy, breakage, and ultimately fiber loss. They employ a variety of state-or-the-art molecular and histological methodologies to elucidate the mechanisms involved in age-dependent muscle fiber loss; the work also examine the accumulation and impact of mtDNA deletion mutations in aged cardiac and brain tissue. Using pharmacological interventions, they have been investigating the underlying mechanism driving the increase in mtDNA deletion mutations with age and the concomitant loss of electron transport activity and ultimately fiber loss.
The loss of muscle mass and function with age is an inevitable component of the aging process. In humans, skeletal muscle fiber number in quadriceps declines from 600,000 at 50 years of age to 323,000 at 80 years. Judd's lab has shown that one cause of this decline in fiber number is the accumulation of mtDNA genomes containing large deletion mutations, and their studies suggest a progression of events beginning with the generation and accumulation of a mtDNA deletion mutation, the concomitant development of electron transport chain, a subsequent triggering of apoptotic and necrotic events, a process resulting in muscle fiber atrophy, breakage, and ultimately fiber loss. They employ a variety of state-or-the-art molecular and histological methodologies to elucidate the mechanisms involved in age-dependent muscle fiber loss; the work also examine the accumulation and impact of mtDNA deletion mutations in aged cardiac and brain tissue. Using pharmacological interventions, they have been investigating the underlying mechanism driving the increase in mtDNA deletion mutations with age and the concomitant loss of electron transport activity and ultimately fiber loss.
Country:
Canada