Scientists have found that both ageing and depression are associated with a biochemical change in a particular gene called the FKBP5 gene.
It has been found by a group of German and American scientists that both ageing and depression are associated with changes in a single gene. The mutation in the FKBP5 gene is also associates with increase in markers of inflammation and cardiovascular risk.
The reason behind age-related diseases, such as cardiovascular diseases and neuropsychiatric disorders being worse in chronically stressed and depressed individuals may be explained based on these findings.
An addition or removal of methyl (CH3) groups to an area of the gene can regulate it. It was found by the researchers that ageing can decrease this methylation process, leading to an over-expressed FKBP5 gene. It was also discovered that when an individual is depressed, this demethylation process is accelerated even further.
Researchers even drew the association between an increased FKBP5 expression with increase 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 study was presented at the European College of Neuropsychopharmacology Congress.
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