🧠 This brain protein might help Alzheimer's spread its damage

In Alzheimer’s disease, the damage does not stay in one place. It gradually spreads to new regions of the brain, with increasing consequences for memory and independence. Researchers believe they have identified a mechanism that could contribute to this progression: a protein called Arc.

Arc is not unknown to neuroscientists. This protein usually plays a role in communication between neurons. However, the team observed that it could also serve as a vehicle for a toxic form of Tau, a protein closely linked to Alzheimer's.

In a healthy brain, Tau contributes to the proper functioning of neurons. The problem arises when it accumulates and forms abnormal clumps. These structures gradually disrupt the cell and can eventually destroy it.

To travel, Arc associates with tiny biological bubbles called extracellular vesicles. These naturally pass from one neuron to another. Toxic Tau appears to be able to take advantage of this journey, like a stowaway, to reach cells that were previously unaffected.

The experiments were conducted in mice that reproduce certain mechanisms of Alzheimer's. In animals lacking Arc, the vesicles contained almost no toxic Tau. The transmission to new neurons then became very weak.

This discovery does not, however, make Arc the ideal culprit. The protein also seems to help diseased neurons eliminate some of the Tau. Without this exit, the toxic substance accumulates more in the initial cell, which then risks dying faster.

The whole difficulty therefore lies in slowing the spread without worsening local damage. Researchers are particularly considering intercepting the vesicles transporting Tau after their release. This strategy would protect neighboring neurons while allowing diseased cells to eliminate part of their toxic load.

Vesicles containing Arc and Tau have also been found in human brain tissue. However, the mechanism still needs to be confirmed in patients. The lead therefore remains preliminary, but it adds an important piece to the puzzle of Alzheimer's progression.