Health
Discovery of key mechanism of Huntington's disease may pave the way to early detection and treatment
Researchers at the University of Oxford have identified a key biochemical mechanism associated with the development of Huntington's disease. This discovery opens up the possibility of studying the disease before clinical onset and ultimately halting its progression.
This research natural metabolism, for the first time revealed the biochemical changes that lead to the development of Huntington's disease and how blocking these changes can halt disease progression.
Huntington's disease is an inherited disease in which parts of the brain stop working properly, causing mental and physical weakness that slowly worsens over time. Symptoms usually begin to appear after age 30 and are fatal, but can worsen over a period of up to 20 years.
The study investigates how early changes described in the brains of HD patients in the early 1980s led to the development of Huntington's disease. Researchers believe that problems with specific neurons in the brain, called indirect pathway spiny projection neurons (iSPNs), are the first cells affected in HD and that important signaling stems from the activation of neurotrophins. It was determined that overlooking this can lead to an imbalance in dopamine levels. Receptor TrkB. This imbalance is associated with early symptoms of the disease, such as abnormal involuntary movements.
First, researchers looked at mice that lacked the normal function of these iSPNs due to disruption of TrkB neurotrophin signaling and noticed that dopamine levels in the brain were elevated, causing hyperactivity. . These changes occur before significant symptoms appear, suggesting that these early changes may significantly contribute to the progression of HD.
The researchers also discovered that a protein called GSTO2, an enzyme that is part of glutathione metabolism, plays an important role in regulating dopamine levels. By selectively reducing the activity of this protein in mice, the researchers were able to prevent dysfunction in dopamine and energy metabolism and prevent the development of motor symptoms in the mice.
Importantly, this enzyme shows similar dysregulation in rat models of HD and in some rare brains of asymptomatic HD patients, supporting the putative link of this enzyme to the development of this disorder. There is.
Liliana Minichiello, lead author of the study and professor of cellular and molecular neuroscience at Oxford University's School of Pharmacy, said: “The big problem with Huntington's disease is that by the time symptoms develop, much of the damage has already been done. “Understanding the changes that occur before the disorder develops is fundamental to developing effective treatments.”
“This study is the first to be able to identify specific chemical changes that are unique to the development of Huntington's disease, giving us an opportunity to study early changes in the disease before irreversible damage occurs.” This opens up the possibility of developing new tests.”
“Understanding these early changes provides important insight into how Huntington's disease develops, and this knowledge may help maintain dopamine balance and slow or halt disease progression. This could be useful in developing preventive treatments.”
Dr Yaseen Malik (School of Pharmacy, University of Oxford), lead author of the paper, said: 'Despite a good understanding of its pathophysiology, HD remains without a cure. This highlights the need for diagnostic and therapeutic intervention before the onset of HD.''This study is a step in that direction. ”
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Sources 2/ https://www.sciencedaily.com/releases/2024/10/241028131900.htm The mention sources can contact us to remove/changing this article |
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