Huntington’s disease research news. In plain language. Written by scientists. For the global HD community.
The largest ever therapeutic trial for Huntington's disease was halted early this week because an analysis of the results to date showed that it was very unlikely to show positive results. The study, called 2CARE, was designed to test whether a treatment called coenzyme Q10 could slow the progression of HD.
The symptoms of HD are caused by damage to the brain, but not all parts of the brain are affected equally. This raises an important question - if we had a treatment that could help only a small part of the brain, which part would we pick? A new mouse study from William Yang, at UCLA, attempts to answer this question.
All the proteins in our body are made of tiny chemical building blocks, called amino acids. The internet was recently buzzing about a newly discovered link between one of these amino acids, cysteine, and Huntington's Disease. Is it true, as some headlines suggested, that "Brain Degeneration In Huntington’s Disease Caused By Amino Acid Deficiency"?
Studies have shown that HD patients tend to get less efficient sleep, fewer hours of sleep, and wake up more times during the night. However, sleep in Huntington’s is under-researched because historically scientists have investigated HD as a disease of movement impairment, and sleep problems don’t seem to have anything to do with movement impairment.
The results are in from the Reach2HD study, which was designed to test the experimental drug PBT2 for early and mid-stage Huntington's disease. The drug seems safe and well-tolerated at the doses that were tested, but we have major concerns about the way the results have been reported.
The results of a new study called PRECREST, investigating whether the nutritional supplement creatine can slow Huntington's disease progression, have just been published. Uniquely, this studied the effects of high-dose creatine supplementation in people carrying the HD mutation, but without clear disease symptoms.
Many types of stresses occur within cells that have the HD gene, and examining how simple organisms cope can help scientists define new targets for HD drugs. A new study examines yeast to determine which proteins can protect these cells from damage and death, uncovering a protective antioxidant and a related drug.
Copper, the metal, may play a role in worsening the symptoms of Huntington’s disease. Bing Zhou and his team looked for connections between HD and the amount of copper in neurons. They report that reducing copper in neurons or keeping it from binding to the HD protein improves symptoms.
Many people in the Huntington's disease community have noticed reports highlighting a recent study from the University of Leicester, which the BBC claimed "could treat Alzheimer's, Parkinson's, Huntington's and other diseases". The underlying study is well-executed research of some importance. However, the press hype is out of all proportion to the impact of this research. What does this study actually show, and what does it mean for HD?