Mitochondrial Mutations Blamed for Aging Alla Katsnelson
Despite the search for the fountain of youth, growing older
remains inevitable. Some biochemical effects of aging are
thought to relate to cell structures called mitochondria,
thousands of which are present in every cell. Mitochondria
are the cell's energy converters and have their own DNA.
Scientists have long known that mutations in mitochondrial
DNA (mtDNA) become increasingly common in older animals, but
they have not been able to determine whether such mutations
are a cause of aging or an effect.
To answer this question, Aleksandra Trifunovic of the
Karolinska Institute in Sweden and her colleagues
genetically engineered a line of mice to carry a compromised
version of an enzyme called DNA polymerase-gamma, which
normally proofreads mitochondrial DNA to ensure proper
replication and aids in DNA repair. Subsequent tests of the
transgenic animals' brain, heart and liver cells revealed
three to five times as many errors in their mtDNA as in that
of normal mice. By 25 weeks of age, young adulthood for
rodents, the mutants began to develop hallmark signs of
aging, including heart problems, osteoporosis, baldness and
reduced fertility. None of them lived more than 60 weeks,
the researchers report today in Nature. Normal mice, in
contrast, live 100 weeks on average. Future experiments can
use the prematurely aging mice to study how growing old "can
be counteracted by genetic, pharmacological, or dietary
interventions," the team writes.
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Posted by Robert Karl Stonjek.