BERLIN / LONDON (IT BOLTWISE) – New research shows that removing the protein centaurin-α1, which is elevated in Alzheimer’s disease, significantly reduces inflammation, plaque formation and cognitive deficits in a mouse model. This discovery could represent a promising therapeutic approach.
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Recent research from the Max Planck Institute has shown that removing the protein centaurin-α1, which is elevated in Alzheimer’s patients, produces significant improvements in an established mouse model of the disease. Eliminating this protein reduced inflammation, reduced plaque formation, and alleviated cognitive deficits. These results suggest that centaurin-α1 may be a promising therapeutic target.
The research team investigated whether genetically removing centaurin-α1 would affect the development of disease symptoms in a mouse model of Alzheimer’s disease. The mice bred without this protein showed a significant reduction in neuroinflammation and an approximately 40% reduction in plaque burden in the hippocampus. This region of the brain is particularly badly affected by Alzheimer’s.
Interestingly, the reduction in plaque formation was not uniform across all brain regions, suggesting that different mechanisms are at work in different areas of the brain. This could mean that successful treatment of Alzheimer’s disease requires a multi-pronged approach. In addition to reducing plaque formation, removal of centaurin-α1 also protected neuronal connections in the hippocampus, leading to improvements in spatial learning.
Researchers are now aiming to find out whether reducing centaurin-α1 in adulthood could also slow disease progression. Initial evidence suggests that loss of centaurin-α1 also led to improvement in symptoms in a mouse model of multiple sclerosis, suggesting that its role in disease progression could be extended to multiple neurodegenerative diseases.
The study highlights the importance of centaurin-α1 as a potential target for future therapeutic development. The normalization of gene expression patterns in the centaurin-α1-deficient mice suggests that this protein may regulate multiple Alzheimer’s-related processes. Researchers plan to further study the role of centaurin-α1 to understand how it worsens the disease and whether reducing it in adulthood might also be beneficial.
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