New research suggests an enzyme found in some brain cells may play a key role in the development of Huntington’s disease.
(Image credit: Shutterstock)
Scientists have identified an enzyme that may play a crucial role in triggering Huntington’s disease, a rare and deadly disorder that causes brain cells to decay.
New research in rodents and humans has shown that the levels of a specific enzyme — glutathione S-transferase omega 2 (GSTO2) — go up in the brain prior to the start of Huntington’s symptoms.
These findings, published Oct. 28 in the journal Nature Metabolism , may point to new ways to head off Huntington’s before it develops, the study’s authors say. Future treatments could include drugs that block GSTO2, to halt or slow the progression of the disease.
Huntington’s disease is an inherited disorder caused by a mutation in a gene called HTT, which carries instructions for a protein called huntingtin. A parent who carries this mutant gene has a 50% chance of passing Huntington’s disease to each child.
Related: Lab-grown ‘minibrains’ help reveal why traumatic brain injury raises dementia risk
The mutation spurs cells to make too much dopamine — a key chemical messenger in the brain — and this causes certain neurons to degrade. This decay is particularly pronounced in a part of the brain called the striatum , causing patients to develop cognitive and movement-related symptoms . These can include difficulty walking, involuntary jerking movements, and trouble focusing.
Huntington’s symptoms typically start to appear in a person’s 30s to 50s . The condition progressively impairs a patient’s ability to function, eventually causing death about 10 to 30 years after symptoms begin.
Get the world’s most fascinating discoveries delivered straight to your inbox.
Until now, scientists haven’t been able to explain why the HTT mutation results in excessive dopamine production. That’s one reason there is no cure for Huntington’s — the available drugs only help to alleviate the symptoms once the damage has been done. The HTT gene is also active throughout the body, making it difficult to develop targeted treatments that combat its effects in the brain.
In the new study, the researchers took a different approach: “Instead of looking at the mutation in this particular gene that causes Huntingon’s disease, we looked at the signals that this mutation affects and what they do,” Liliana Minichiello , lead author of the study and a professor of cellular and molecular neuroscience at the University of Oxford, told Live Science.
Information contained on this page is provided by an independent third-party content provider. This website makes no warranties or representations in connection therewith. If you are affiliated with this page and would like it removed please contact editor @americanfork.business
