The fusion of ruptured vesicles containing alpha-synuclein protein, in green, leads to the formation of large protein clumps resembling the proteins that form in the brains of Parkinson's disease patients. Photo by Loyola University Chicago
May 23 (UPI) -- Researchers have discovered that abnormal proteins in common neurodegenerative diseases share the same ability to cause damage in brain cells.
The study by Loyola University in Chicago found that Alzheimer's, Parkinson's, Huntington's and other neurodegenerative disorders share a critical feature that causes damage when invading brain cells.
Neurodegenerative diseases are caused by the death of neurons and other cells in the brain. Different diseases typically affect different regions of the brain, such as Alzheimer's destroying memory and Parkinson's and Huntington's affecting movement.
Brain damage from neurodegenerative diseases comes from proteins that are folded abnormally and form clumps inside brain cells. The clumps spread from cell to cell causing them to die. Each neurodegenerative disease involves different proteins being affected such as tau in Alzheimer's, alpha-synuclein in Parkinson's and huntingtin in Huntington's disease.
Researchers found that once proteins get inside a cell, they enter vesicles, or small compartments that are encased in membranes. The proteins then damage or rupture the vesicle membranes allowing the proteins to invade the cytoplasm and cause more damage.
Loyola researchers discovered that the protein clumps associated with Alzheimer's, Parkinson's and Huntington's diseases cause the same type of vesicle damage.
The findings could lead to an effective treatment for one neurodegenerative disease might work for other neurodegenerative diseases.
"A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," Dr. Edward Campbell, a researcher at Loyola University, said in a press release. "If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases."
The study was published in the journal Acta Neuropathologica.