Researchers from the University of Copenhagen have discovered a hitherto unknown error in the transport of glutamine between astrocytes and neurons in the brains of mice with Huntington’s disease.
In a new study, researchers from the Novo Nordisk Foundation Center for Protein Research and the Department of Drug Design and Pharmacology at the University of Copenhagen (published in Cell Reports), describe how an important exchange between astrocytes and neurons in the brain is disturbed during Huntington’s disease – more precisely, the glutamate-GABA-glutamine cycle. According to the researchers, this highlights the important role of astrocytes in the brain.
The researchers have analyzed the protein alterations seen in the four regions of the brain – striatum, cortex, hippocampus and diencephalon – in mice with advanced Huntington’s disease compared to healthy mice and found that the striatum, as in humans, was more affected than the other regions of the brain. The researchers found a total of around 900 protein alterations. This was supported by the researchers’ metabolic studies, which also showed a majority of disorders in the striatum.
The most important find of the study is the reduced exchange of glutamine between astrocytes and neurons. This is a research area with potential when it comes to future research into whether a normal release of glutamine from the astrocytes can potentially alleviate the symptoms of Huntington’s disease.
“Even though Huntington’s disease is a genetic disease, our study shows a dysregulation of the proteins and the signaling pathways of these proteins. There is currently no cure for Huntington’s disease. But if we were able to find areas in which the effects of the disease may potentially be improved or reduced, it would be a big step in the right direction. This study may provide suggestions for focus areas of future research,” says Professor Michael Lund Nielsen.