New Delhi: Premature aging in Down's Syndrome could be caused by an overactive gene on chromosome 21 that disturbs the DNA-damage-repair mechanisms, leading to accelerated aging, according to a new research.
An overactivity of the gene, called DYRK1A, on enzymes that quicken chemical reactions in the body disturbed the DNA-damage-repair mechanisms, causing cells to develop more DNA damage and become more fragile, thereby accelerating the aging process, the research led by Queen Mary University of London, UK, found.
Adults having Down's Syndrome, caused by being born with an extra copy of chromosome 21 or with trisomy 21, have been known to exhibit early signs of conditions associated with the biological process of aging such as reduced tissue regeneration capacity, delayed wound healing, osteoporosis, senescence of the brain and immune cells, among others.
Further, people having this non-heritable genetic disorder were biologically older than their chronologically-aged counterparts by 19.1 years, on an average, and that the premature ageing process starts very early in childhood, this study published in the Lancet Discovery journal eBioMedicine found.
"We have uncovered that trisomic overdose of this gene (DYRK1A) is one of the main contributors to premature biological ageing in Down's Syndrome.
"Further research is needed to understand how much this contributes to brain development and function, and also in finding ways of precisely inhibiting the overdose of this gene back to physiological levels," said lead researcher Dean Nizetic, professor of cell and molecular biology.
The research also showed that limiting this gene's activity could potentially correct the cellular ageing defects, opening up possibilities for early therapeutic interventions for people having Down's Syndrome.
Studying genetically caused accelerated aging may help us understand aging mechanisms better and devise strategies to slow down the ageing process, the study said.
Down's Syndrome affects around 7 million people worldwide.