The Brain's Helper Cells: When Protection Turns into a Blow bioRxiv

Original: "Differential Associations of Microglial Inflammation on LATE-NC and Tangle-Related Hippocampal Atrophy"
b42w:2608.90036 · the paper's page · 2026-08-27 · CC BY 4.0 · 1 min
The brain's immune cells don't destroy memory on their own, but they make the damage from the TDP-43 protein worse.

In an orchestra, the conductor doesn't play a single instrument, yet the loudness of the music depends on them. The same goes for the brain's immune cells, called microglia: they don't start the disease, but they can make its blow harder.

Scientists took the brains of 441 people who had donated them to science after death. The average age of these people was 90 years. The brains were scanned with a tomograph to measure the hippocampus, the region that stores memories. Then thin slices were stained to reveal microglia, and a computer counted these cells. It turned out that if the TDP-43 protein accumulates in the brain, then the more microglia there is, the smaller the hippocampus. But for Alzheimer's proteins, there is no such link.

It's as if the fire brigade showed up to every call, but with one type of fire they accidentally soaked the furniture, while with another they worked carefully.

So drugs that calm microglia may help not everyone, but only those who have TDP-43 in their brain. For now, such people are hard to find while alive, but scientists are looking for ways. And then treatment will become not "for everyone" but "for those who need it."

The average age of participants at death was 90.1 years, and the average duration of education was 16 years. These are among the oldest and best-educated cohorts in the world.

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Concepts
inflammation microglia alzheimers disease