Additionally, the researchers demonstrated that RPS23R1 also exerts its function in human cells, suggesting that RPS23R1 signaling pathways are active in humans. "While it is not yet known whether there are functional analogs of RPS23R1 in humans, further elucidation of RPS23R1 functions and mechanism of action may prove to be important for developing new strategies for combating AD and other diseases, including cancer and diabetes, in which the PKA and GSK-3 signaling pathways are centrally involved," concludes Dr. Xu.

The authors also reported that the mouse Rps23r1 gene, whose human counterpart has not yet been identified, was created during evolution through a process called retroposition, in which a gene is "duplicated" through the reverse transcription of mRNA and the "duplicate" is placed in a different location in the cell's DNA. Although most retroposition events result in non-functional duplicates (called pseudogenes), in rare cases, retroposed genes, like Rps23r1, can become functional.

"From the point of view of treating Alzheimer's disease, if we can express the mouse gene in human brain cells, we may be able to control the buildup of amyloid beta and tau neurofibrillary tangles," said Dr. Xu. "From an evolutionary point of view, we have found an example of a retroposed gene that took on a completely new function."

Source: Cell Press