Study identifies protein that accelerates development of Alzheimer's

A new study published in the journal Cell reveals the mechanism that the Arc protein uses to accelerate the development of Alzheimer's in the brain. The research is led by the University of Utah, in the United States.

The tau protein is mainly responsible for the development of Alzheimer's. In people who have the disease, this protein becomes deformed, creating tangles that kill brain cells. The big mystery was knowing how it "jumps" from a sick cell to a healthy cell.

Results of research carried out at the University of Utah revealed that the Arc protein works as a packager, creating small capsules or "bubbles" (scientifically called extracellular vesicles) and placing the toxic tau protein inside them. The neuron then shoots these bubbles out.

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What makes this discovery relevant is why the neuron does this. According to the researchers, the cell is trying to save itself: it realizes that the tau protein is toxic and tries to "throw out the trash" to avoid its own death.

This rubbish, however, does not disappear. The capsules stay in the brain and are absorbed by healthy neurons. Once inside the new cell, the Alzheimer's seed begins to spread again, infecting the rest of the brain's circuitry.

The discovery may explain why many drugs tested to date have not worked. Therapies try to use antibodies to "clean up" the tau protein that floats between cells, but because it is hidden inside these bubbles (vesicles) created by Arc, drugs can't reach it.

Brain bubbles
By analyzing the brains of patients who died from Alzheimer's, researchers confirmed that the more Arc protein there was in these brain "bubbles", the greater the amount of toxic tau present.

These results open a new avenue for treatment: if scientists can find a way to stop the Arc gene from packaging the tau protein, they could, for the first time, halt the progression of the disease through the nervous system.

In the research, brain tissue samples from 15 individuals were analyzed: seven Controls (without the disease, between 59-90 years old), one Patient at an early stage (Braak stage 2) and seven Patients with advanced Alzheimer's (Braak stage 6, between 62-90 years old).

The study is considered highly comprehensive as it covers multiple levels of biological complexity, including molecular and computational levels, cellular levels, organismal levels and clinical validation.

*Under the supervision of Thiago Félix

Source: CNN