WASHINGTON, June 14:
A widely-used anti-malaria drug may help prevent hearing loss caused by heredity and genetic disorders, a study has found.
Researchers from Case Western Reserve University in the US conducted a study on zebrafish with a commonly used anti-malarial drug called artemisinin.
They found that the drug can help sensory cells of the inner ear recognise and transport an essential protein to specialised membrane using established pathways within the cell, which will help improve and restore hearing.
The ability to hear depends on these proteins reaching the outer membrane of the sensory cells in the inner ear which may be hindered due to certain types of mutations in the protein due to hereditary disorders, which prevent it from reaching those membranes.
The sensory cells of the inner ear are covered by hair-like projections, called hair cells, on the surface.
These hair cells convert vibrations from sounds and movement into electrical signals that are conveyed through the nerves and translated in the brain into information for hearing and balance.
The genetic mutation of the protein — clarin1 — makes hair cells unable to recognise and transport the signals to the membrane and gets trapped inside the hair cells where they are harmful to the cells.
This faulty secretion of clarin1 most commonly occurs in the Usher syndrome, which causes hearing and vision loss.
The study, published in the Proceedings of the National Academy of Sciences (PNAS), found that artemisinin restores cell function of the inner ear — and thus hearing and balance — in genetically engineered zebrafish that have human versions of the essential hearing protein.
“We knew mutant protein largely fails to reach the cell membrane, except patients with this mutation are born hearing. This suggested to us that, somehow, at least a fraction of the mutant protein must get to cell membranes in the inner ear,” said Kumar N Alagramam from Case Western Reserve University.
“If we can understand how the human clarin1 mutant protein is transported to the membrane, then we can exploit that mechanism therapeutically,” Alagramam said. (PTI)
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