A gene called MSH3 helps to repair our DNA, but in HD it can slip up and cause CAG repeats to lengthen. Researchers have uncovered new information about how MSH3 activity is controlled, opening the door to new therapeutic avenues.
CAG repeats expand in some parts of the body and brain as people with HD get older, a phenomenon known as somatic instability. Learn more about how researchers are exploring somatic instability and DNA repair to design therapies for HD.
A collaborative team of scientists from Canada and Japan have identified a small molecule which can change the CAG-repeat length in different lab models of Huntington's disease. #HuntingtonsDisease #DrugDiscovery
HDBuzz reports from the annual Huntington’s disease therapeutics conference in Palm Springs
Multiple teams find small differences in the 'CAG repeat' bit of the Huntington's disease gene. They don't directly change the huntingtin protein, but do alter the age of symptom onset. What's behind this enigma and what does it mean for patients?
DNA takes centre stage for day 2 of the Huntington's Disease Therapeutics Conference in Palm Springs
A surprising new paper sheds light on the role of the HD gene early in development. Should we worry?
Two recent studies show how a cellular border control system goes wrong in HD, opening new avenues for HD research.
Huntingtin helps fix damaged DNA, a recent study suggests, under the direction of a gene repair protein called ATM.