A recent study succeeded in identifying a new group of genes that play a role in increasing the possibility of Parkinson’s disease, which is the second most common denial neurological diseases after Alzheimer’s.
The study was conducted by researchers from the University of North Western in the United States of America, and published on April 10 in the magazine “Sains”, and wrote about the “Yorik Alrt” website.
The study relied on a sophisticated technology called “CrisPR Interference” to examine all genes in the human genome, a system used to disable part of the DNA without cutting it, which opened the door to developing new treatments targeting biological paths that were not previously known.
The puzzle remained in the research of Parkinson’s disease is the difference in the response of individuals carrying the pathogenic mutations, as some of them suffer from the disease while others remain healthy despite their pregnancy of genetic mutations themselves.
The genetic mutations that cause Parkinson’s disease
The prevailing theory indicates that this contrast may be due to the interaction of additional genetic factors that interfere in determining the course of the disease, as it acts as modified factors either to accelerate the appearance of symptoms or to protect those of these mutations from infection.
This study revealed a group of 16 protein known as “Commander”, which works together in a cellular path that was not previously known, as it was found that these genes play a decisive role in transferring certain proteins to Lysosomes, which are parts of the cell that act as recycling centers, as they dismantle unwanted materials.
Previous research has shown that the mutations in a gene known as “GBA1” (GBA1) represents the largest risk factor for Parkinson’s disease and dementia accompanied by Louie bodies, as these mutations reduce an activity of an enzyme called “Glucocerebrosidase”, which is the enzyme responsible for the cellular recycling process in the status particles, but that Mystery remains the cause of the injury of some of these mutations, while others remain immune to the disease.
In this context, the current study discovered a new mechanism that explains this difference, as the researchers focused on the group of “Kumander” genes that play a decisive role in organizing the activity of the enzyme Glucoserprosidase inside the status of the status, and by analyzing the genetic data of two large groups of patients, scientists noticed the presence of disrupted mutations in the “Kumander” genes in people with Parkinson’s disease compared to healthy people.
The study showed that the imbalance in the function of the status is a common feature of many denial neurological diseases, which makes targeting “Kumander” genes is a promising therapeutic choice, as the researchers suggested that medications that enhance the work of this compound may improve the function of the status, which may slow the development of the disease.