Researchers at the Van Andel institute (Grand Rapids, MI, USA) have developed a new laboratory model of Parkinson’s disease that could give scientists an idea of what occurs in the brain years before motor symptoms appear. The model demonstrates the gradual spread of abnormal alpha-synuclein proteins, which are strongly associated with Parkinson’s disease.
By the time symptoms of Parkinson’s disease appear, more than half of brain cells involved in the production of dopamine have died. Although it is currently unknown what triggers this process, evidence suggests a combination of genetic, epigenetic and environmental factors, with strong evidence proposing that clumps of abnormal alpha-synuclein are involved in the disease process.
“Better models that mimic the early stages of the disease will allow us to more precisely study Parkinson’s, and by extension, find new ways to potentially stop it before it progresses,” mentioned lead author Nolwen Rey (Van Andel Research Institute).
She continued: “Our model replicates the phase that occurs long before diagnosis and, importantly, gives us a powerful tool to test novel interventions that might prevent the onset of Parkinson’s.”
The study, published in the Journal of Experimental Medicine, demonstrates that alpha-synuclein travels along nerve cells in the olfactory bulb before the initial motor symptoms, suggesting that this area may be susceptible to the spread of alpha-synuclein, eventually causing deficits in the sense of smell. Alpha-synuclein then reaches additional brain regions, including the area of the brain stem that houses dopamine cells.
“…we have created a model of prodromal Parkinson’s disease, the condition that precedes the diagnosis of the disorder in humans by five to 10 years,” commented senior author Patrik Brundin (Van Andel Research Institute). “The model will prove invaluable when testing novel therapeutics designed to slow down or stop the progression of disease.”
Sources: Rey NL, Steiner JA, Maroof N, et al. Widespread transneuronal propagation of α-synucleinopathy triggered in olfactory bulb mimics prodromal Parkinson’s disease. The Journal of Experimental Medicine, DOI: 10.1084/jem.20160368 (2016) [Epub ahead of print]; Van Andel Research Institute press release