Why cells age: the culprit is the courier service inside them ✎ bioRxiv

Original: "Attenuating LRRK2 activity ameliorates progerin-induced aging phenotypes in HGPS models and during physiological aging"
b42w:2608.90079 · the paper's page · 2026-08-07 · All rights reserved · independent analysis · 1 min
The same protein makes cells age faster both in the rare disease progeria and in ordinary elderly people.

Inside every cell there is its own courier service. Tiny bubbles, like little trucks, deliver proteins to the right addresses. If the service breaks down, the cargo gets stuck, and the cell starts to age. This is exactly what happens in the rare disease progeria: children with it age several times faster than usual.

Scientists have found that the breakdown is caused by a protein called LRRK2. It acts like a dispatcher who pushes the couriers too hard. The transport system collapses under the overload: the cell nucleus loses its protective shell, and damage appears in the DNA. When LRRK2 was switched off in cells from progeria patients and from elderly people, the cells started to look young again.

In worms whose version of this protein was switched off, life got longer and their movements in old age were livelier.

The most interesting part: drugs that calm LRRK2 are already being tested for Parkinson's disease. If they also work against aging, elderly people could stay healthy longer.

Progerin differs from normal lamin A by the absence of just 50 amino acids, yet that is enough for the protein to get permanently 'stuck' to the nuclear membrane and set off a cascade of aging.

Take the whole work

Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.

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