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An unexpected source of inflammation in the brain in Alzheimer"s disease discoveredScientists have made an important discovery in understanding the mechanisms of Alzheimer"s disease development, finding a previously unknown source of inflammation in the b

An unexpected source of inflammation in the brain in Alzheimers disease discoveredScientists have made an important discovery in understanding the mechanisms of Alzheimers disease development, finding a previously unknown source of inflammation in the b

Breakthrough in Alzheimer's Disease Research: Scientists Reveal the Mechanism of Brain Inflammation

A team of researchers from the University of California has made an important discovery in the field of neurodegenerative diseases. Scientists have established that proteins involved in the formation of characteristic plaques in Alzheimer's disease directly trigger inflammatory processes in the brain. The results of this significant study were published in the prestigious scientific journal Proceedings of the National Academy of Sciences (PNAS).

The scientists focused on amyloid precursor proteins (APP), which later form beta-amyloid peptides that create toxic plaques. Researchers identified the surprising ability of APP to interact with special proton channels Hv1, which control the function of microglia – the brain's immune cells. These cells perform a protective function, but their excessive activation can lead to destructive inflammation and damage to nerve tissue.

When APP or its fragments (particularly the C99 segment) connect with Hv1 channels, their activity increases. As a result, microglia begin to produce elevated levels of inflammatory molecules. Researchers also discovered that when APP concentration decreases, channel activity and inflammatory processes are significantly reduced.

Particularly important was the observation that patients with hereditary mutations in the APP gene, which cause an early form of Alzheimer's disease, show significantly increased activity of these channels. This discovery may explain why inflammatory processes in the brains of such patients develop with greater intensity and speed.

"We've long known that Hv1 controls inflammation, but we didn't expect the APP protein to directly affect its function. This unexpected discovery shows how we can more precisely target these channels when treating neurodegenerative diseases," noted the study's senior author David Goldstein.