(RxWiki News) Swedish researchers have found that damaged alpha-synuclein proteins can spread in Parkinson's disease similar to an infection model found in conditions like mad cow disease.
The finding contributes to greater understanding of the development of neurodegenerative diseases. The discovery may even lead to new treatments by inhibiting this cell-to-cell spread and slowing down "the relentless disease progression and worsening of symptoms in patients," said Professor Patrik Brundin.
Professor Brundin, of Lund University, Sweden, who led a team of investigators from research centers in Denmark, France and Portugal, said the discovery marks considerable progress in deciphering the potential role of cell-to-cell transfer of alpha-synuclein in Parkinson's disease pathogenesis (development).
This transfer can aggravate alpha-synuclein in recipient cells as well, possibly marking "an important mechanism for the spread of the pathology," according to Dr Christian Hansen, one of the key investigators in the study.
Six months after Parkinson's disease model mice were transplanted with healthy dopamine neurons, researchers discovered that new brain cells contained human alpha-synuclein, which points to cell-to-cell transfer from the host brain to the transplanted neurons.
As many as one million Americans live with Parkinson's disease, according to the Parkinson's Disease Foundation. That's more than the combined number of people diagnosed each year with multiple sclerosis, muscular dystrophy and Lou Gehrig's disease (known as ALS).
