The long -term treatment of Parkinson’s disease usually brings trouble of trouble: non -voluntary, unstable exercise, which significantly affects the quality of life of patients. These motion complications are called L-Dopa-induced motor disorders, which has always been a continuous challenge in managing Parkinson’s disease. However, recent research reveals a potential solution that can reduce these weakened impacts and bring new hope to people affected by this chronic disease.
Researchers have made great progress in solving the long -term treatment related to Parkinson’s disease (PD). Professor Heinz Steiner, Dr. FERAS Altwal, Dr. Connor Moon and Rosalind Franklin’s Anthony West of Medical and Science University, explored the impact of multi-mode serotonin Vilazodone on L-Dopa-induced genetic adjustment to reduce the PD animal model alleviating Motor disorder. Their discovery was published in the “magazine” magazine.
Parkinson’s disease is a neurodegenerated disease characterized by dopamine loss of neurons, which is usually treated with L-DOPA. Although L-DOPA is still a gold standard treatment method, its long-term use can cause motor disorders caused by L-DOPA. This disease is marked by non-voluntary and unstable exercise. Motor disorders will seriously damage the quality of life of PD patients because it makes the treatment benefits of L-DOPA complicated.
The research team surveyed Vilazodone, the antidepressant characteristic of the US Food and Drug Administration (Vilazodone). The drug will combine the effect of selecting the inhibitors (SSRI) with the 5-HT1A receptor activity. Essence Their research involves a recognized PD animal model, of which rats use 6-oxyl dopamine (6-OHDA) for unilateral dopamine consumption. The rats are then treated with L-DOPA alone or combined with Vilazodone for three weeks.
Professor STEINER said: “Our most important conclusion is that Vippizole ketone effectively suppresses the development of motor disorder caused by L-DOPA without interfering with the beneficial exercise effect of L-DOPA.” Researchers found that L-Dopa Treatment has significantly improved the expression of certain genes, such as Dynorphin, 5-HT1B and ZIF268 mRNA, on the same side of the lesions. Pipoprazole ketone coincides with these neurons, which shows that anezoleone can alleviate the targeted mechanism of disconnected disorders.
These discoveries also emphasize that the effect of hpoprazole is a direct way to dopamine infiltrate the pattern, because it does not affect the integrated pathway in the middle of the complete tattoo or the brain expression in gene expression. This specificity is essential for developing auxiliary therapy. These treatments can reduce symptoms without damage the effect of the main treatment methods.
Professor Stanner pointed out: “These results are positioned as a potential auxiliary drug to treat the side effects induced by L-DOPA induced in Parkinson’s disease in Parkinson’s disease. Pay the way for the new treatment strategy. “
All in all, research by Professor STEINER and his colleagues shows that Piprazole ketone can effectively reduce the lina-Dopa induced motor disorder. This is a common and weak side effect in PD treatment without damage the therapeutic effect of L-Dopa’s therapeutic effects Essence These promising results show that the anthrazole ketone, which has been approved as a antidepressant, can be re-used to improve the quality of life of PD patients treated with L-DOPA. Future research will focus on verifying these findings in clinical trials to explore the long -term benefits of Vilazodone as part of PD management.
Journal reference
Altwal F., Moon C., West AR, Steiner H. “Multi-mode serotonin Vilazodone inhibits the genetic regulation of L-DOPA-induced in neurons in the neurons, and inhibit the relevant related animal models in the Parkinson’s disease model “Sexual barrier” cells. 2020. Doi: https: //doi.org/10.3390/cells9102265
About the author
Dr. Henz Stanner It is a professor of cells and molecular pharmacology at the University of Chicago Medical College, a professor of cells and molecular pharmacology at the University of Medicine and Sciences of Rosalind Franklin University. Dr. Steiner obtained a master’s degree in biology from the Swiss Federal Technology Institute (ETH) and his doctoral degree from Zurich, Switzerland. Ph.D. in physiological psychology at the University of Dusseldorf, Germany. After the postdoctoral work of the Institute of Psychological Health of the Bessel, he was a research assistant professor at the Department of Anatomy and Neurological Biology at the University of Tennessee, the School of Medicine and Memphis. He joined the Department of Honeycomb and Molecular Pharmacology at the Chicago Medical College in 2000, and served as the director of the department from 2011 to 2022. Dr. STEINER’s research focuses on the functional tissue of the base ganglia and related brain systems, especially the role of neurotransoprotic dopamine and 5-hydroxylidine in the adjustment of the base ganglia-cortex interaction. One of the main goals of his work is to understand how dopamine and 5-hydroxylidin drug treatment methods cause changes in genes regulating genes and their consequences of drug addiction and other brain diseases. Dr. STEINER is a senior editor of the “Base Conduct Structure and Function Handbook”, and is also the co -editor of Elsevier’s “Behavior Neuroscience Manual” series.
