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New Hypothesis Unites Brain-First and Body-First Models in Parkinson’s Disease

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A new hypothesis paper published on World Parkinson’s Day by researchers from the University of Rochester Medical Center and Aarhus University Hospital in Denmark aims to bridge the long-standing debate on the origins of Parkinson’s disease. The study proposes a unified theory that combines the brain-first and body-first models, suggesting that environmental toxicants play a key role in the development of the disease.

The debate over whether Parkinson’s disease originates in the brain or the body has divided the scientific community for years. The groundbreaking hypothesis integrates these two theories, linking the toxic proteins implicated in the disease to environmental factors such as inhaled and ingested toxicants.

According to the researchers, environmental toxicants like certain pesticides, dry cleaning chemicals, and air pollution can trigger the formation of toxic proteins that are central to the pathology of Parkinson’s disease. These toxicants can enter the body through inhalation or ingestion, leading to distinct pathways of disease onset.

The brain-first model suggests that inhaling toxic chemicals, such as trichloroethylene (TCE) and perchloroethylene (PCE), can result in the spread of toxic proteins from the brain’s smell center to other regions, including dopamine-producing neurons. On the other hand, the body-first model posits that ingested toxicants can initiate pathology in the gut’s nervous system, eventually affecting both sides of the brain and spinal cord.

Key environmental toxicants implicated in the hypothesis include the weed killer paraquat, common dry cleaning chemicals, and air pollution. These toxicants have been linked to the formation of toxic proteins like alpha-synuclein, which are associated with the progression of Parkinson’s disease.

The authors underscore the systemic nature of Parkinson’s disease, highlighting the role of the nose and gut as potential starting points for the disease. They emphasize that environmental exposures, combined with genetic and other factors, may determine an individual’s susceptibility to developing Parkinson’s.

This new model not only sheds light on the potential causes of Parkinson’s disease but also paves the way for preventive strategies. By elucidating the role of environmental toxicants in the onset of the disease, the researchers hope to advance understanding and ultimately prevent Parkinson’s and related brain disorders.

Rachel Adams

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