Blocking Bach1 Protein Slows Down Degeneration Of Parkinson’s Disease Brain Cell

Researchers discovered a novel drug that helps to protect vital neurons against inflammation and toxic stress that propels symptoms of Parkinson’s disease (PD).

Scientists are investigating all the aspects possible to find ways to improve treatments for Parkinson’s disease, which is a neurodegenerative condition that affects more than 10 million people across the world. A new study conducted by a team of scientists at Medical University of South Carolina discovered a protein that plays an important regulatory role in the neurodegeneration related conditions. The study published in the journal Proceedings of the National Academy of Sciences on October 25, 2021 found that Bach1 proteins were increased in autopsied brains affected with PD and cells that did not contain Bach1 were protected from the damages that occur in PD.

The research focused on a protein pair that controls the gene activity, Nrf2 and Bach1 protein. The team conducted experiments on engineered mice with Parkinson’s disease. To protect neurons that produce dopamine from destruction associated with stress, the team removed Bach1 from the equation and studied the genomes of the mouse brain to find out activated genes. The researchers found that Bach1 represses the protective genes’ expression that are usually controlled by Nrf2 as well as it also controls expression of numerous other genes that are not directly controlled by Nrf2.

Furthermore, to create a drug HPPE that inhibits Bach1 as well as activates Nrf2, the team partnered with a pharmaceutical company named vTv Therapeutics. When the drug was tested in mice, it was found that the drug is capable of alleviating symptoms when administered before or even after onset of the disease as it switches on the antioxidant genes and turns off the genes that promote inflammation. The team now plans to investigate further to explore effects of long-term HPPE use and its potential in treatment of other neurodegenerative conditions.