A significant discovery that could pave the way for a new treatment for Parkinson's disease was made by researchers.
The findings focus on an enzyme known as parkin, whose absence causes an early-onset form of Parkinson's disease.
Precisely how the loss of this enzyme leads to the deaths of neurons has been unclear.
But The Scripps Research Institute (TSRI) researchers showed that parkin's loss sharply reduces the level of another protein that normally helps protect neurons from stress.
"We now have a good model for how parkin loss can lead to the deaths of neurons under stress," TSRI Professor Steven I. Reed, who was senior author of the new study, said.
"This also suggests a therapeutic strategy that might work against Parkinson's and other neurodegenerative diseases," he said.
Parkin belongs to a family of enzymes called ubiquitin ligases, whose main function is to regulate the levels of other proteins.
They do so principally by "tagging" their protein targets with ubiquitin molecules, thus marking them for disposal by roving protein-breakers in cells known as proteasomes.
Because parkin is a ubiquitin ligase, researchers have assumed that its absence allows some other protein or proteins to evade proteasomal destruction and thus accumulate abnormally and harm neurons.
The research is published online in the journal Molecular and Cell Biology.