Scientists have found that both ageing and depression are associated with a biochemical change in a particular gene.
The change in the FKBP5 gene is also associated with increases in markers of inflammation and cardiovascular risk, researchers said.
The finding may explain why risk for ageing-related diseases, such as cardiovascular diseases and neuropsychiatric disorders, are worse in chronically stressed and depressed individuals.
Genes can be regulated by the addition or removal of methyl (CH3) groups to an area of the gene.
The researchers from Germany and the US found that ageing can decrease this methylation process, causing the FKBP5 gene to be overexpressed. They also found that when someone is depressed, this demethylation process is accelerated even further.
Researchers also found that this increased FKBP5 expression is associated with increases in biochemical markers of inflammation and cardiovascular risk.
"We found that both ageing and depression seem to lead to changes in how DNA is processed, and that this can control the expression of genes that regulate how we respond to stress," said lead researcher, Dr Anthony Zannas from Max Planck Institute of Psychiatry, Munich.
"These changes are associated with increased inflammation, and we believe that this may lead to the increased risk for several aging-related diseases, such as cardiovascular diseases and neuropsychiatric disorders, that has been observed in chronically stressed and depressed individuals," Zannas said.
"Our work shows that risk for ageing-related diseases could be conferred by epigenetic changes of stress-related genes and resultant increases in the expression of inflammation markers.
"It's too early to say that we are seeing a cause and effect, so we need to confirm the findings by using larger samples and uncover the mechanisms using animal models," Zannas said.
The FKBP5 gene is found on chromosome 6 in humans. It codes the FK506 binding protein 5, also known as FKBP5. This protein is known to play a role in stress responses, immune regulation and basic cellular processes involving protein folding.
The work was presented at the European College of Neuropsychopharmacology Congress here.
