The impact of environmental factors on the development and progression of Parkinson’s disease has long been studied, but a recent research study sheds light on a new potential risk factor: noise exposure. A study published in PLOS Biology by Pei Zhang and colleagues from the Huazhong University of Science and Technology in Wuhan, China, explores the effects of high-volume noise exposure on a mouse model of early-stage Parkinson’s disease.
The researchers exposed mice with early-stage Parkinson’s disease to acute and chronic loud noise, ranging from 85 to 100 decibels. This level of noise is comparable to the sound of a power mower or a blender. The results were striking – after just one hour of noise exposure, the mice exhibited motor deficits and reduced balance compared to control mice. With continued exposure to noise for one hour per day over a week, the early-stage Parkinson’s mice displayed chronic movement problems.
Further investigation revealed a connection between the auditory processing area of the brain, specifically the inferior colliculus, and the substantia nigra pars compacta, a region responsible for dopamine production that is severely affected in Parkinson’s disease. Chronic activation of the inferior colliculus mimicked the behavioral effects of noise damage in the Parkinson’s mouse model, leading to a reduction in a protein called VMAT2, which transports dopamine, and the death of dopamine-producing cells in the substantia nigra.
Interestingly, inhibiting the inferior colliculus or increasing VMAT2 levels reversed the harmful effects of noise exposure in the early-stage Parkinson’s mice. This highlights the potential role of environmental factors, such as noise, in exacerbating Parkinson’s disease pathogenesis.
While the study was conducted in a mouse model, and additional research is needed to fully understand the implications for humans, these findings suggest a crucial link between sound processing areas of the brain and regions damaged in Parkinson’s disease. The authors emphasize the importance of considering environmental factors in the management and treatment of Parkinson’s disease, noting that noise exposure could be a non-genetic risk factor for the illness.
In conclusion, this study provides valuable insights into the impact of noise exposure on Parkinson’s disease progression and symptoms. By uncovering the mechanisms through which noise affects movement and neuronal vulnerability in a Parkinson’s mouse model, researchers can pave the way for future studies investigating the role of environmental factors in neurodegenerative diseases.
