Neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease, affect different regions of the human brain. Despite these regional differences, research has shown that the processes inside cells affected by these diseases have a lot in common. One characteristic of these diseases is that specific proteins start to form aggregates, or deposits, that damage and eventually kill the cell. In Parkinson's disease, it is misfolded forms of a protein known as α-synuclein that are involved. These aggregates can recruit normal forms of α-synuclein, causing the formation of more protein aggregates.
"During the past few decades, we have realised that the protein deposits in the brain can spread between cells, acting as seeds that start a new aggregation cycle in the next cell. The disease in this way spreads in the brain in a manner similar to an infection. We want to understand how the protein spreads, and use this knowledge in the long term to inhibit the spread of disease in the brain," says Martin Hallbeck, associate professor in the Department of Clinical and Experimental Medicine at Linköping University and consultant in surgical pathology at Linköping University Hospital.
Cells - Channels - Gap - Junction - Channels
It has long been known that cells that lie close to each other can create small channels (known as gap junction channels) between them. These small channels are built from members of a family of proteins known as connexins. Studies by other scientists have suggested that connexins play a role in other types of disease, such as HIV/AIDS. This led the researchers at Linköping University to wonder whether connexins can play a similar role in the spread of Parkinson's disease in the brain.
"It turned out that the harmful protein aggregates in Parkinson's disease can bind to connexin-32, Cx32, and be absorbed by a cell. We are the first to demonstrate that connexins play a...
Wake Up To Breaking News!
Freedom is Never Free!