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Mother link to faster ageing

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OUR SPECIAL CORRESPONDENT Published 04.09.13, 12:00 AM

New Delhi, Sept. 3: Genetic mutations inherited from the mother may speed up ageing, contributing to premature loss of hair, greying of hair and even a hunchback, a new study in mice has suggested.

The study by a team of scientists in Germany, Sweden and the US is the first to show that mutations in a genetic material called mitochondrial DNA present in the egg and inherited exclusively from the mother can influence the pace of ageing.

While earlier studies have implicated dysfunction of the mitochondria — the power houses of cells — in heart failure, diabetes and neurodegenerative diseases, the scientists say their research points to a new mechanism that can accelerate ageing.

“We find that genetic mutations inherited only from the mother can aggravate and possibly predict ageing,” said Jaime Marie Ross, a post-doctoral research fellow at the Karolinska Institute, Stockholm, the first author of the study published last month in the journal Nature.

The mitochondrial DNA is passed down by mothers to both male and female offspring and can affect both in the same way. “Our findings suggest that if we inherit mutations from our mother, ageing can progress faster,” Ross told The Telegraph over the telephone.

The researchers observed a variety of age-associated features in the animals with the inherited maternal mitochondrial DNA mutations.

“In our animals, we saw hair loss, greying of hair, hearing loss and reduced ability to move,” said Nils-Goran Larsson, director of the Max Planck Institute for Biology of Ageing at Cologne in Germany, a senior member of the research team.

While the studies were conducted on laboratory mice and the same mechanisms are likely to occur in humans, Larsson told this newspaper, the findings would need to be validated.

“The results are surprising because we really didn’t think a modest amount of mutated mitochondrial DNA would become visible as a mice ages,” said Lars Olson, a senior neuroscientist at the Karolinska Institute and a member of the research team.

The experiments concentrated on two sets of mutations — mutations in the mitochondrial DNA and a mutation in a specific gene that plays a role in proof-reading the replication of the mitochondrial DNA.

The study revealed that if mice are born with mutations in the mitochondria and also carry this mutation in the proof-reading gene which adds to mitochondrial mutations, about a third of the live-born mice have brain malformations.

“It takes two hits — starting life with mutations in the mitochondrial DNA and inheriting mutations in the proof-reading gene — to impair brain development,” Olson said in an interview via email.

A team member in the US said the results suggest that therapeutic interventions that target mitochondrial functions may influence the pace of ageing.

“There are various dietary manipulations and drugs that can influence mitochondrial function and reduce mitochondrial toxicity,” Barry Hoffer at the Case Western Reserve University School of Medicine said in a media release issued by his institution.

“One example would be anti-oxidants,” Hoffer said. “This mouse model would be a platform to test the effects of such drugs or diets.”

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