Berlin, July 01 (QNA) - Scientists at the Leibniz Institute on Aging - Fritz Lipmann Institute have identified a previously unknown mechanism underlying cellular aging, finding that a gradual decline in the production of phosphatidylcholine impairs the function of mitochondria -- the cell's energy-producing structures -- and contributes to age-related cellular deterioration.
Mitochondria generate the chemical energy required for cells to grow and perform essential biological functions. The researchers found that age-related reductions in phosphatidylcholine, a major lipid component of mitochondrial membranes, disrupt the integrity and flexibility of the mitochondrial network, reducing the cells' ability to distribute energy efficiently.
The team combined experiments in human tissues, cultured human cells and laboratory models to investigate the effects of gradually reducing phosphatidylcholine production. Their findings showed that lower levels of the molecule weaken mitochondrial membranes, leading to fragmentation of the mitochondrial network and a decline in cellular metabolic flexibility.
The researchers also found that phosphatidylcholine levels were lower in people with diabetes and obesity, while higher levels were associated with indicators of healthy aging, including faster walking speed and better memory. Human metabolomic data further showed that phosphatidylcholine levels decline gradually in men but fall more sharply in women around menopause.
"You can imagine the whole system as a finely branched power grid that becomes increasingly damaged with age: connections break down and currents stall," said Maria Ermolaeva, the study's senior author at the institute. "Although energy production continues, it becomes less efficient and sustainable, and energy can no longer be distributed flexibly."
The study concluded that declining phosphatidylcholine synthesis is a previously unrecognized driver of natural mitochondrial aging. The researchers said restoring phosphatidylcholine levels through dietary supplementation may help preserve mitochondrial function and slow aspects of cellular aging, although further studies are needed to determine whether the findings translate into effective treatments for humans. (QNA)