Year of selection 2015
Institution Max-Planck-Institute for Biology of Ageing
By the time you read this text, it will have been proofread by an editor. Your cells, too, rely on proofreading to catch any mistakes that may have occurred when copying the entirety of their DNA before cell division. But typos can slip past the most careful of readers, and some such cellular errors may be intimately linked to ageing. Dr. Francesca Baggio is exploring this scenario for a special kind of DNA that is housed in a cell’s mitochondria. These structures are the site of energy production and are unique for possessing their own genetic material, called mtDNA. In previous studies, mice with a defective mtDNA-proofreading system showed an accumulation of errors—and premature ageing. Dr. Baggio wants to know if this same phenomenon underlies the normal ageing process. If so, she might find a way to delay its onset and allow people to live longer in good health.
Working with fruit flies, which use a similar enzyme to mammals to ensure mtDNA proofreading, she will assess whether individuals live longer when they accumulate fewer errors. Genetic studies will allow her to search for new molecules that alter the way ageing occurs by increasing or decreasing this enzyme’s activity. By clarifying the link between dysfunctioning mitochondria and ageing, Dr. Baggio hopes to understand better how the process occurs and to reveal fundamentally new targets for the treatment of age-related diseases. The burden of such conditions is huge and increasing every year. Dementia, for instance, affected some 44 million people worldwide in 2014—a number that is expected to triple by 2050. Its estimated cost of $604 billion in 2010 has nowhere to go but up, unless preventative treatments can be found. Dr. Baggio’s research could open doors to new ways of tackling these age-related challenges that are at once medical, economic and societal.
Scientific title: Identification Of Novel Genes Modulating Age-Associated Mitochondrial Dysfunction
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