A study has found that abnormal proteins found in Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease all share a similar ability to cause damage when they invade brain cells.
The finding potentially could explain the mechanism by which Alzheimer’s, Parkinson’s, Huntington’s, and other neurodegenerative diseases spread within the brain and disrupt normal brain functions. The study was published in Acta Neuropathologica.
Previous research has suggested that in all three diseases, proteins that are folded abnormally form clumps inside brain cells. These clumps spread from cell to cell, eventually leading to cell deaths. Different proteins are implicated in each disease: tau in Alzheimer’s, alpha-synuclein in Parkinson’s and huntingtin in Huntington’s disease.
The researchers focused on how these misfolded protein clumps invade a healthy brain cell. The authors observed that once proteins get inside the cell, they enter vesicles (small compartments that are encased in membranes). The proteins damage or rupture the vesicle membranes, allowing the proteins to then invade the cytoplasm and cause additional dysfunction.
The researchers said the finding that protein clumps associated with the three diseases cause the same type of vesicle damage was unexpected. The researchers, who are based in the U.S., initially focused on alpha-synuclein proteins associated with Parkinson’s disease. They asked a French collaborator known for his ability to generate distinct types of alpha-synuclein to send them different types. Without telling the researchers, the collaborator sent other types of proteins as well. This led to the surprise finding that tau and huntingtin proteins also can damage vesicles.
Paper: “Endocytic vesicle rupture is a conserved mechanism of cellular invasion by amyloid proteins”
Reprinted from materials provided by Loyola University Health System.