Prof. Siegfried Hekimi
Fellow
Current Employer
McGill University
Election Year
2010
Academy
Académie des sciences
Discipline
Molecular Biology and Genetics
Department
Department of Biology
Keywords
Aging, genetics, mitochondria, age-dependent diseases, lipoproteins
Hekimi, Siegfried - Molecular Biology and Genetic - McGill University
Siegfried Hekimi has advanced our understanding of the causes of animal aging, in particular by discovering and studying long-lived mutants and using them to test theories of aging. For example, his work suggests that free radicals might not be the cause of aging, in contrast to what was previously widely believed.
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Hekimi, Siegfried - Molecular Biology and Genetics - McGill University
Siegfried Hekimi’s work has advanced our understanding of the mechanisms that dictate animal longevity. He has contributed significantly in pioneering and validating the genetic approach to the study of aging using nematodes and mice. Specifically, his work has demonstrated that: 1) There are evolutionarily conserved genes whose function limits lifespan, 2) Such aging genes can be grouped into independent genetic pathways, 3) There is a positive causal relationship between mitochondrial electron transport and aging. 4) Molecular damage from mitochondrial reactive oxygen species is not the link between mitochondrial function and aging.
Siegfried Hekimi has advanced our understanding of the causes of animal aging, in particular by discovering and studying long-lived mutants and using them to test theories of aging. For example, his work suggests that free radicals might not be the cause of aging, in contrast to what was previously widely believed.
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Hekimi, Siegfried - Molecular Biology and Genetics - McGill University
Siegfried Hekimi’s work has advanced our understanding of the mechanisms that dictate animal longevity. He has contributed significantly in pioneering and validating the genetic approach to the study of aging using nematodes and mice. Specifically, his work has demonstrated that: 1) There are evolutionarily conserved genes whose function limits lifespan, 2) Such aging genes can be grouped into independent genetic pathways, 3) There is a positive causal relationship between mitochondrial electron transport and aging. 4) Molecular damage from mitochondrial reactive oxygen species is not the link between mitochondrial function and aging.
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