Parkinson’s spread mechanism revealed

British researchers have uncovered the process by which Parkinson’s disease spreads from cell to cell, it was announced last night.

Researchers at Oxford Parkinson’s Disease Centre, England, said their stem cell research is the first to link the release of alpha synuclein (a naturally occurring protein that is important in the development of Parkinson’s) with GBA1, its most common genetic risk factor.

Professor Richard Wade-Martins, head of Oxford Parkinson’s Disease Centre, and lead researcher on the Parkinson’s UK-funded study, describes in Stem Cell Reports how the team studied stem and brain cells from a group of people with Parkinson’s who carry the GBA1 genetic mutation and from a control group without the condition.

They discovered that the GBA1 mutation creates problems with how proteins, particularly alpha-synuclein, are processed and recycled in cells. This leads to a build-up of alpha synuclein, which is released into the brain, thereby contributing to the spread of Parkinson’s.

Prof Wade-Martins said the discovery opens new possibilities for new treatments that could help to stop excess alpha-synuclein being released into the brain.

“Thanks to this study, for the first time we know how the protein is released, giving us new clues on how this spread happens,” he said.

“Most importantly, these findings open up new avenues into investigating potential new therapies or treatments that could stop the spread of alpha-synuclein and slow the condition’s progression.”

Dr Arthur Roach Parkinson’s UK director of research, added: “This study is a good example of how studying a genetic form of the condition can provide important insights into what is thought to be a fundamental feature of all forms of Parkinson’s.”

Fernandes et al, ER Stress and Autophagic Perturbations Lead to Elevated Extracellular a-Synuclein in GBAN370S. Parkinson’s iPSC-Derived Dopamine Neurons, Stem Cell Reports. February 2016. [abstract]

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