United States: A new study has found an important chemical change in the brain that causes Huntington’s disease. Scientists were able to change this process, which helped prevent symptoms in animals. This discovery could ultimately lead to early treatments and therapies to stop the disease from getting it even more worse.
Discovery for Huntington’s Disease
As reported by Scitechdaily, today’s study in Nature Metabolism now reveals the first-ever biochemical shift that directly triggers Huntington’s disease and reveals that turning off this shift will prevent the disease’s progression.
Huntington’s disease is a genetically inherited disease that causes chronic decline of mental ability and motor function in the afflicted patient. Symptoms genera
lly appear after 30 years of age and progress over 10–20 years to be fatal.
First Altered Development of Huntington’s Disease
The change that was studied concerns a proteolysis first observed in the Huntington’s patients in the beginning of the 1980s and which may trigger the disease. It was established that disruption of the dopamine balance is caused by dysfunction of the direct pathway spiny projection neurons (iSPN), which are among the first cells that are affected by Huntington’s illness.
This disruption takes place when the neurotrophic receptor TrkB is not activated correctly, resulting in the early manifestation of the illness characterized by involuntary and abnormal movements.
First, the researchers observed mice with impaired iSPN function because of mutated TrkB neurotrophin signalling and found that hyperactive levels of dopamine existed in the animals’ brains. This conversion took place prior to clinical signs, implying that these modifications may well play a role in HD development.
Protein Regulation for Diseases
The researchers also discovered that GSTO2 situated in glutathione metabolism is involved in dopamine homeostasis. By selectively knocking down this protein in mice, the researchers have avoided the dysfunction of dopamine and energy metabolism and have halted the development of motor symptoms in mice.
However, this enzyme exhibits identical abnormalities in a rat model of HD and several exceptional brains of presymptomatic HD individuals, thus enforcing their hypothesis that this enzyme is associated with the emergence of the disease.