There is something highly unusual about Brooke Greenberg’s DNA. Perhaps unique in fact.
Brooke is a 17-year-old girl who – outwardly – became “frozen” when she was one year old. Her development appeared to stop abruptly and, aged 17, she still has the body and behaviour of an infant.
Weighing just 16lb and at 30in tall, tiny Brooke is like a baby who simply never grew up.
For 17 years, Brooke’s parents, Howard and Melanie Greenberg, have cared for their little girl in exactly the same way. In their home in Reisterstown, Baltimore, they feed her, change her nappies, cuddle her and put her to sleep early each evening. Still their baby after all these years, Brooke can smile and crawl but she hasn’t learnt to talk and she still has her baby teeth.
Now geneticists have her parents’ permission to study Brooke’s DNA in an attempt to discover why she has not developed as other humans do. Researchers expect that as well as throwing light on Brooke’s arrested development, their studies may add to the growing body of knowledge about youth, health and ageing.
Preliminary examination of her DNA indicates that Brooke’s failure to develop and age normally may result from defects in certain genes that lead the rest of us to develop, mature and grow old.
Paradoxically, while Brooke has remained an infant in many ways she has also suffered numerous life-threatening conditions more commonly seen in older people. Among other health problems, she has had strokes, fits, ulcers and respiratory problems which would not normally be seen in a teenager. Rather than uniformly halting Brooke’s ageing process, the flaws in her genes have provoked an ageing process which is dramatically uneven.
Richard Walker, a professor at the University of South Florida School of Medicine, is leading the research on Brooke’s DNA. He says: “Brooke’s condition presents us with a unique opportunity to understand the process of ageing. We think that she has a mutation in the genes that control her ageing and development so that she appears to have been frozen in time. If we can compare her genome to the normal version then we might be able to find those genes and see exactly what they do and how to control them.”
On the possible consequences of such research he adds: “If we can use her DNA to find that mutant gene then we can test it in laboratory animals to see if we can switch if off and slow down the ageing process at will. Just possibly it could give us an opportunity to answer the question of why we are mortal.”
In our commercially-minded, youth-obsessed world, the holy grail of this type of research would undoubtedly be therapy to slow ageing without provoking health problems. Imagine the profits accruing to companies able to halt ageing and prevent age-related disease.
Other researchers chasing that prize are working at the opposite end of the human life span from Brooke’s. Eline Slagboom is a professor of molecular epidemiology at Leiden University in Holland. Her research on ageing is with families whose members live to a great age. She gathered data on thousands of people from long-lived families to analyse the genetic and other factors that give them long lives.
These people age more slowly than others, she says. They have firmer, healthier skin and fewer age-related diseases like diabetes, heart disease and high blood pressure. Their metabolism also works more efficiently.
And so, she asks: “What is controlling [this slower] ageing? So far, the evidence suggests that there could be just a few key genes in charge of it all. If we can find out where they are and how they work, it opens the way to new therapies against the diseases of ageing that could work in all of us.”
So Brooke, who has not aged normally, and the old people who have aged more healthily than others, may hold the key to understanding and then manipulating the ageing process. Wouldn’t it be great if the research and eventual therapies could be driven by the health and social needs of humans and not the dollar signs in corporate eyes? What’s the betting?