Huntington’s disease research news. In plain language. Written by scientists. For the global HD community.
Recent days have seen a torrent of news stories about a new technology, called CRISPR, which has been described as having potential application in Huntington's disease. Is this new technique as cool as it sounds? Possibly — but, as always, the truth is more complicated than the headlines suggest.
Huntington’s disease (HD) progression is a long process in which the first changes in the brain happen well before we even see symptoms in patients. It makes sense to focus our efforts on treating the earliest changes, to nip the problem in the bud. But what are these changes and how can we target them? A recent study has literally shed some light on this question. By creating HD mice with glowing brain cells, researchers at the University of Nottingham Medical School and the Babraham Institute in the UK have found that some of the earliest changes happen before these cells start to die, in a region of the brain where HD researchers have never before thought to look.
Antibodies, produced by the body’s immune system to fight off infection, can also be used by scientists to study proteins. A new antibody has provided new insights into what causes neurons to die in Huntington's disease.
The mutant huntingtin protein forms clumps, or aggregates, in brain cells. Many scientists believe these clumps contribute to the death of these cells and symptoms in HD. Now scientists have used a beam of neutrons to study the earliest structures formed in these aggregates.
Build-up of unwanted chemicals in cells is one way the HD mutation causes damage to neurons. A cellular recycling process called autophagy is crucial to getting rid of these harmful chemicals. Now researchers have found a way of identifying safe drugs that can increase the rate of garbage disposal in HD.