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Targeted Therapies for Various Diseases on the Anvil
The tRNAs, assemble amino acids for the production of proteins within mitochondria. If in case the mitochondrial tRNA genes are defective or missing, and proteins are not manufactured, the mitochondria are unable to generate adequate energy.
It is believed that defective tRNAs are the cause of about 60 percent of conditions traced to malfunctions in the mitochondria, like diabetes, hearing loss and a number of neurological disorders, depending on which kinds of cells are affected.
As the Mitochondria are encased in their own membrane, it becomes a complicated structure to study. Previous research has suggested that only in lower organisms, such as protozoans, yeast and plants, can tRNAs be imported to the mitochondria from the cell cytoplasm. But in this new research, scientists determined that tRNAs can be imported from cytoplasm to mitochondria in rat liver cells and human cells as well.
"This was totally unexpected, to find an innate, built-in mechanism that we humans have," said Juan Alfonzo, senior author of the study and an assistant professor of microbiology at Ohio State University.
He said that the finding broadens the study of therapeutic options involving attempts to introduce healthy tRNAs to the defective mitochondria of ill patients.
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