Brown mouse Credit: Understanding Animal Research
Cambridge scientists have shown how the brain's ability to clear out toxic proteins is impaired in Huntington's disease and other forms of dementia - and how, in a study in mice, a repurposed HIV drug was able to restore this function, helping prevent this dangerous build-up and slowing progression of the disease. Brown mouse Credit: Understanding Animal Research We are very excited about these findings because we've not just found a new mechanism of how our microglia hasten neurodegeneration, we've also shown this can be interrupted David Rubinsztein A common characteristic of neurodegenerative diseases such as Huntington's disease and various forms of dementia is the build-up in the brain of clusters - known as aggregates - of misfolded proteins, such as huntingtin and tau. These aggregates lead to the degradation and eventual death of brain cells and the onset of symptoms. One method that our bodies use to rid themselves of toxic materials is autophagy, or -self-eating-, a process whereby cells -eat- the unwanted material, break it down and discard it. But this mechanism does not work properly in neurodegenerative diseases, meaning that the body is no longer able to get rid of the misfolded proteins. In a study published today in Neuron, a team from the Cambridge Institute for Medical Research and the UK Dementia Research Institute at the University of Cambridge has identified a process that causes autophagy not to work properly in the brains of mouse models of Huntington's disease and a form of dementia - and importantly, has identified a drug that helps restore this vital function.
TO READ THIS ARTICLE, CREATE YOUR ACCOUNT
And extend your reading, free of charge and with no commitment.
