Scientists Identify Mechanism Reversing Cellular Aging Rate

Scientists at the Fritz Lipmann Institute have discovered a previously unknown mechanism of mitochondrial aging. They found that as organisms age, the level of phosphatidylcholine in cells decreases, leading to the deterioration of these cellular "power stations."

The journal Nature Communications reports that, according to the researchers, this lipid can be replenished through diet.

The study involved the use of C. elegans worms, human tissue samples, and human cells as models. Across all three systems, the researchers observed a gradual inhibition of phosphatidylcholine synthesis with advancing age. This lipid is a fundamental component of the outer mitochondrial membranes; its absence reduces membrane flexibility, causes mitochondrial fragmentation, and disrupts energy distribution within the organelles.

Biologist Maria Yermolayeva described the process metaphorically: "One can imagine the entire system as a branching electrical network that gradually deteriorates with age—connections break and currents weaken."

Tatyana Polizayeva, head of the research team, noted that when phosphatidylcholine or choline (its dietary precursor) was added to the worms' diet, their mitochondria regained a more vital and flexible state.

She stated, "We were surprised by the extent of this molecule's impact on mitochondrial structure, connectivity, and function."

Analysis of human tissue samples revealed two significant findings:

First, the decline in phosphatidylcholine levels was more pronounced in patients with diabetes and obesity, while higher levels correlated with brisk walking and good memory—both indicators of healthy aging.

Second, the lipid level decreased gradually in men but dropped sharply in women approaching menopause, which may explain the sudden energy decline experienced by many women during this period.

The researchers emphasize that phosphatidylcholine deficiency is only one factor in mitochondrial aging but an important one. Correcting this deficiency through diet offers a practical pathway to slow cellular aging.