Different people live in the same house. Some age quickly, some slowly. The brain is the same way: cells of different types age differently. Some disappear early, others hold out until the end of life. For a long time scientists didn't understand why. Now they have looked inside each cell and found its own internal clock. These clocks don't run the way the body's master clock does.
To see this, the scientists took the brains of 69 people of different ages and measured gene activity in each cell separately. They built a model that first predicted a person's age from general features, then refined the prediction for each cell. That's how they separated the age of the whole brain from the age of an individual cell. It turned out that cells that look younger by their own clocks are more likely to die during aging and in Alzheimer's disease.
Scientists compared this data with the genes of 240 animal species. In long-lived species, the dangerous stretches of genes are more often switched off, as if evolution itself shuts them down. Now we know which cells need protection first. This will help create drugs that save vulnerable brain cells.
In long-lived mammalian species, the regulatory regions linked to neuronal vulnerability are more often closed, meaning evolution seems to 'switch off' dangerous stretches of the genome. The MIR181A1HG locus has kept its connection to its enhancer for hundreds of millions of years across mammals, birds, and reptiles, which points to its ancient and important function.
The idea of molecular clocks that predict cell vulnerability echoes the film Blade Runner, where replicants have a limited lifespan but the vulnerability of different organs and cells is not the same. In Greg Egan's novel Permutation City, the possibility of controlling aging at the cellular level is discussed, which partly reflects the goal of this work.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.