Ample new details about a key protein implicated in early-onset forms of Parkinson’s disease published this week in Science answer many questions and should further help propel the search toward new medical treatments, the researchers believe.

It was already known that in healthy persons, mitochondria-protecting protein PINK1 senses damaged mitochondria in the energy factories of cells. It then attaches itself to the damaged organelles and tags them for clearance.

Damaged mitochondria stop making energy and start releasing toxic by-products into the cell, while in a person with Parkinson’s disease with a mutation in PINK1, damaged mitochondria pile up in the brain cells, and the release of toxins eventually kills the cell.

Now, it had further been known that PINK1 mutations would cause Parkinson’s disease, particularly in young adults.

But up until this point, no one had described what the protein looks like or its mechanism of action.

“The first time we’ve been able to see human PINK1 anchored to the surface of damaged mitochondria…” study co-author Dr. Sylvie Callegari of the Walter and Eliza Hall Institute at the University of Melbourne in Australia said in a statement. “We also saw for the first time how mutations found in people with Parkinson’s disease affect human PINK1.”

“After learning what the protein looks like, how it binds to mitochondria, and how it is activated, this gives rise to many new ways to think about modifying PINK1 so as to turn its activity on, which will have life-changing effects upon those with Parkinson’s disease,” said study leader David Komander from the same institute in a statement.