Lewy body diseases, like Parkinson’s disease and dementia with Lewy bodies, are characterized by the presence of Lewy bodies (deposits of a misfolded but naturally-occurring protein called alpha-synuclein), and a depletion of the neurotransmitter (chemical messenger) dopamine. The majority of dopamine-producing cells die before motor symptoms of Parkinson’s disease emerge. But until now, research has not demonstrated whether the presence of Lewy bodies is linked to the cascade of symptoms in Parkinson’s.
The first hints of cell-to-cell transmission of Lewy body pathology came in 2008. Researchers transplanted fetal nerve tissue into the brains of individuals with Parkinson’s disease and years later discovered the transplanted cells developed the same pathology. Subsequent research demonstrated that this cell to cell transmission led to cell death. But questions remained as to how Lewy body pathology caused the progressive devastation of Parkinson’s disease.
Researchers at the University of Pennsylvania led by neurobiologist Virginia M.-Y Lee, director of the Center for Neurodegenerative Disease Research, have now discovered that when mice have a synthetic version of misfolded alpha-synuclein injected into the brain, there is a cell to cell transmission of the rogue protein to the nerve cells near the injection site and the development of Parkinson’s-like Lewy body pathology in the brain. This transmission of Lewy body pathology resulted in a progressive loss of dopamine-producing cells and loss of motor function in the mice.
“The spreading of Lewy bodies we have demonstrated for Parkinson’s disease most likely occurs in Lewy body diseases as well, stated Dr. Lee. “Halting this transmission will have therapeutic implications.”
This study, published in Science, provides crucial understanding of how Lewy body pathology spreads and may spur further research into the development of antibodies as treatment strategies for Lewy body diseases.