Causes - Dr. Joel Watts, Professor - Chasing the culprit in Parkinson’s disease
Dr. Joel Watts, Professor
Strains of alpha-synuclein aggregates
When Joel Watts was 10 years old, his father died of Creutzfeldt-Jakob Disease (CJD), a rare brain disorder caused by the strange behaviour of a class of proteins called prions. These agents later became notorious as the cause of the now infamous brain-wasting condition dubbed “mad cow disease”.
But Watts, whose father died in the early 1990s, did not connect his father’s loss to any specific neurodegenerative disorder until much later, when he was studying at university. Today, the biochemistry professor at the University of Toronto is on the cutting edge of investigating the similarities between prions and the way other proteins spread through the brain and compromise its functions.
“What I’m trying to do is take something that is known about prion disease and apply it to Parkinson’s research,” Watts says.
Instead of prions, he studies a protein called α-synuclein, which is directly involved in the development of Parkinson’s. The comparison with prions lies in the way accumulations or clumps of α-synuclein spread throughout the brain.
“This aggregate might start in one cell and then somehow get out of that cell and make its way into a neighbouring cell,” says Watts. “These little pieces of aggregated protein can then start the process in the next cell.”
Just as the mis-folded arrangement of prions damages brain cells, so too does the shape of α-synuclein affect brain cells and contribute to Parkinson’s disease. Watts is categorizing these various shapes and their role in the development of this disorder. His ultimate goal is to shed light on mechanisms that a new therapy could target.
Watts emphasizes that the infectious diseases prions cause, such as CJD, are entirely distinct from brain disorders like Alzheimer’s or Parkinson’s, which have never been identified as contagious or communicable. Nevertheless, Watts remains eager to build on the body of knowledge that surrounds prions, which he believes will lead to fresh insights about Parkinson’s.
“With prions, the protein exists on the outside of the cell so it’s very easy for it to touch another cell,” he says. “Whereas α-synuclein is inside the cell, so how does it get out of one cell and get into another cell? That’s one of the hottest areas of research right now.”