Scientists at the Fritz Lipmann Institute have discovered a previously unknown mechanism of mitochondrial aging. As we age, the level of phosphatidylcholine in cells decreases, leading to the deterioration of these "cellular power plants".
Nature Communications indicates that, according to scientists, this lipid can be compensated for through nutrition.
The researchers used C. elegans worms, human tissue samples, and human cells as models. In all three systems, they observed one thing: a gradual inhibition of phosphatidylcholine synthesis with age. This lipid is a fundamental building block of mitochondrial membranes; without it, the membranes lose their elasticity, the mitochondria disintegrate, and energy distribution within them is disrupted.
Biologist Maria Yermolayeva metaphorically describes the process, saying: "The whole system can be imagined as a branching electrical network that gradually deteriorates with age—the connections break, and the currents weaken."
Tatiana Polizaeva, head of the research team, points out that when phosphatidylcholine or choline (its nutritional precursor) was added to the worms' food, the mitochondria returned to a more vital and flexible state.
"We were surprised by the extent to which this molecule affects the structure, cohesion, and function of mitochondria," she says.
Analysis of human tissue samples revealed two important findings.
phosphatidylcholine were more pronounced in patients with diabetes and obesity, while high levels were associated with brisk walking and good memory - both indicators of healthy aging.
accelerated sharply in women as they approached menopause - which may explain the sudden drop in energy that many women experience during this period.
Researchers emphasize that phosphatidylcholine deficiency is only one factor in mitochondrial aging, but it is an important one, as correcting it through diet ensures a realistic path to slowing down cell aging.
