People are fascinated by folks who make an effort to follow their own rules on appearance and mannerisms - so half of this Guardian piece is taken up with a discussion of Howard Trevor Jacobs' taste in clothing rather than the minor details of his research and acceptance of the Descartes prize. This fellow is one of the scientists organizing and contributing to recent important insights into the role of mitochondrial DNA damage in aging.
His multinational project, which involves scientists from Britain, Italy, Finland and France, promises not only to help in the creation of treatments for a host of illnesses, including deafness and diabetes, but to achieve the Holy Grail of medical science: a way to extend healthy human life.
Mitochondria are the power packs of the cell, with their own DNA, separate from the genes that direct the growth of rest of our bodies. As Jacobs puts it: 'Mitochondrial genomes are the cinderellas of genetics - you inherit them through the maternal line, and no one in science pays them much attention.'
Or that was the case. Thanks to work by Jacobs and other groups, it has been found that errors in mitochondrial genes can lead to the development of various inherited conditions, and that understanding their role offers an opportunity to correct these flaws.
Moreover, experiments using mice bred to accumulate high numbers of errors in their mitochondrial DNA produced startling results. The mice, aged less than a year, acquired a hunchback appearance. They also suffered from hair loss, osteoporosis, loss of fertility, heart disease and brain changes such as those seen in humans with Parkinson's disease.
In short, they got senile although only a few months old. 'This will lead to a much fuller understanding of ageing, and to rather straightforward ways of prolonging a healthy lifespan,' said Jacobs.
There are still some notes of caution to sound with respect to this work - just because you can produce what looks like accelerated aging in mice doesn't mean you have the keys to an extended healthy life span. The next step (already underway) is to build the tools needed to repair and regenerate mitochondrial DNA in mice. Then we can see if this a truly a path to greatly extended healthy life spans. Personally, I am cautiously optimistic - there is a fair weight of science behind the theories backing this sort of work.