Jay Nataro of the University of Tokyo and the Center for Neurodegenerative Disease Research at Nagoya University.
Nataro and his team looked for channels regulated by ADAR1 and abnormal ADAR1 expression in cultured cells to see if such channels might be therapeutic targets for Parkinson’s.
The researchers report that the ADAR1-targeting compound was found in both healthy and Parkinson’s-affected mice.
This observation was fully reproduced in patients with Parkinson’s and AD retrotransposon-lik gene mutations.
They also report finding the compound in a fatty acid that altered ADAR1 expression and reduced ADAR1 function—and this confirmed to be the case in patients with AD.
The researchers suggest that ADAR1 inhibition may be beneficial for patients with Parkinson’s—it has been found that inhibition prevents toxic bleeding through Parkinson’s membrane involving an ion channel known as ‘Melanine-transferrin transmembrane protein 1 receptor’ (TTP1R), which is thought to cause AD.