New insights into mechanisms of Parkinson’s disease
Latest studies on laboratory animals conducted by researchers at the German Center for Neurodegenerative Diseases (DZNE) in Bonn reveal new pathogenic mechanisms of Parkinson’s disease. Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. We already know that a key role in the development of Parkinson’s disease is represented by the protein ‘alpha-synuclein’ that aggregates and accumulates in neurons affecting different areas of the brain. Pathogenic mechanism underlying this degenerative disease is not fully known but one hypothesis is that it may result from an abnormal protein spreading along nerve tracts of the nervous system.
Now experiments conducted by researchers from the German Center for Neurodegenerative Diseases (DZNE) in Bonn provide new keys about the mechanisms of this disease. They created a new experimental model to reproduce the formation of ‘alpha-synuclein’ in neurons. They were able to reproduce the formation of human alpha-synuclein in rats and track the spread of this protein in the lower parts of the brain to the upper parts. The new experimental model could be the basis for the development of therapies to halt the progression of Parkinson’s disease.
Parkinson’s disease is a disease of the nervous system characterized both by motor symptoms (akinesia, motor disorders, tremors, etc.) but also by non-motor symptoms (trouble sleeping, depression, behavioral disorders, etc.). There have not been yet found a drug to cure Parkinson’s disease until the present, but there is treatment to control symptoms and to slow someway disease progression, such as dopamine agonists.
The causes are related to both genetic factors and environmental factors, although the exact cause of this disease is not known exactly. An interesting finding regarding the possible etiology of the disease was that of Friedrich Lewy, a German neurologist, who first discovered that the brains of patients with Parkinson’s disease contain some neuronal inclusions that accumulate progressively (and which were called Lewy bodies).
Studies so far have shown that the formation of alpha-synuclein aggregates begin in “medulla oblongata”, that is in the lower areas of central nervous system and then these aggregates migrate in midbrain and in cortical areas, which referes to more rostral brain regions. To learn more about these aggregates, researchers monitored the production and localization of human alpha-synuclein in rats’ brains over a period of approximately 4 months after injection of viral particles. It was found that the production of human alpha-synuclein occurs only in neurons connected to the vagus nerve, and the overproduction of this protein occurs in conditions of aging, neuronal injury, genetic polymorphisms that might promote Parkinson’s disease.