Key Alzheimer's protein blocked by researchers


Monday, 20 May, 2019


Key Alzheimer's protein blocked by researchers

Researchers from Sweden’s Lund University have shown the de facto key role played by the protein galectin-3 in Alzheimer’s disease, demonstrating a reduction in plaque and inflammatory load after the protein was blocked in mice. Their work has been published in the journal Acta Neuropathologica.

Among other things, Alzheimer’s disease involves the accumulation of amyloid plaques outside cells and tau protein forming lumps within nerve cells. When our innate immune defence system discovers the plaques, the brain’s immune response is activated. It is in precisely this mechanism that the galectin-3 protein appears to play a major role.

“The problem is that if this inflammatory response goes on for a long time, it creates a toxic environment which eventually leads to the breakdown and death of the nerve cells — and the onset of disease,” explained Antonio Boza-Serrano, from Lund University’s experimental neuro-inflammation laboratory.

Galectin-3 is produced by the brain’s sanitation workers, the microglial cells, whose care of the brain’s immune system includes cleaning out harmful proteins that accumulate in the brain. It seems that galectin-3 is required to activate the microglial cells in the case of plaque formation in the brain.

“We have found that this inflammatory protein increases tenfold in the brains of deceased patients with Alzheimer’s disease, and we especially find it in the microglial cells that accumulate around the amyloid plaques,” Boza-Serrano said.

Galectin-3 is also involved in inflammation in the case of Parkinson’s disease and after a stroke. The fact that the protein is barely detectable in healthy brains but increases in cases of inflammation is good from a drug perspective, according to the researchers, as they do not want to risk a drug affecting cells other than those specifically responsible for the development of the disease. It is indeed possible to slow the effect of galectin-3 by using inhibitors that prevent the protein from being active in inflammation.

“We grew microglial cells in the lab and added the protein present in Alzheimer’s plaques, which made the cells become very active from an inflammation perspective,” said Tomas Deierborg, head of research at the experimental neuro-inflammation laboratory. “But when we added the galectin-3 inhibitors, the microglial cells became milder, less inflammatory.”

The researchers were also able to study mice with Alzheimer’s but lacking the gene that produces the galectin-3 protein. They observed that these mice did not develop as much inflammation as those with both Alzheimer’s disease and the galectin-3 gene. When the mice were placed in a labyrinth, those with Alzheimer’s but no galectin-3 had a better memory than the mice with Alzheimer’s and galectin-3.

The researchers acknowledge that the studies in which they inhibited the protein were conducted on cells, and the studies on the lack of the galectin-3-gene were conducted on mice. Nevertheless, Deierborg said they are hopeful that their findings could lead to future treatments for Alzheimer’s disease in humans.

Image credit: ©stock.adobe.com/au/Bulat

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