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.

Read the rest at Scientific American
http://cl.extm.us/?fe8b13717c63047b73-fe3016707360067c711779

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