A team of researchers from the School of Veterinary Medicine conducted a novel study, in which they recognized a protein in the body that can break down compounds into MTPT-like chemicals inside the brains. The compounds are derived from the alkaloids present in specific foods and tobacco, which trigger a neurodegenerative disorder in mice.
The researchers proposed that the enzyme, mitochondrial CYP2D6, can possibly be used a better target for the treatment of Parkinson’s disease.
The paper based on this research is available on the Journal of Biological Chemistry. The study explores the actual mechanism that leads to Parkinson’s disease when the focus is not set at a particular cause.
In previous studies, the researchers had shown that the enzyme CYP2D6, formed in the mitochondria, could play an important part in breaking down MPTP to MPP+. However, in the new study, they thoroughly examined the toxins beta-carbolines and isoquinolines, which look almost similar to MPTP.
The researchers identified that mitochondrial CYP2D6 was the key activator of beta-carbolines and isoquinolines inside the dopamine-secreting neurons, instead of glial cells. This activation mechanism in a mouse model leads to oxidative stress and neuronal damage. Moreover, the scientists demonstrated that mice in which levels of CYP2D6 were not adequate, did not exhibit the severe symptoms associated with Parkinson’s disease.
On a similar subject, scientists from King’s College London have discovered the initial signs occurred in the brain, which are linked to Parkinson’s disease. The signs appear many years before the symptoms shown in the patients.
The study findings are available in the journal The Lancet Neurology. The recent outcomes oppose the traditional diagnostic methods of the disease and could possibly design screening tools for recognizing people, who will be at higher risk.
According to the study, the first evidence of the development of Parkinson’s disease is the secretion of serotonin chemical in the brain.