Parkinson’s disease (PD) is the fastest growing neurological disorder, and as such, this session was of the utmost importance. This session was full of diverse viewpoints and a plethora of information on PD, and I found it extremely relevant to our ever-changing landscape of neuroscience. We heard talks from an epidemiologist, academia researchers, and researcher in the nonprofit sector that really helped give an overall picture of PD research. As someone who researches neurodegenerative disease, I thoroughly enjoyed this session and found it full of great information.
The session began with epidemiologist Samuel Goldman from the University of California San Francisco. Parkinson’s has been around for quite some time and depicted in early texts but was fully described in 1817 by James Parkinson. Parkinson’s is increasing widely in China, where the population is aging rapidly. Environment is a major contributor to PD and presents epidemiological challenges, such as misdiagnosis and the fact that exposure may take place decades before it manifests clinically. The talk went through several case studies, such as the FAME study, an epidemiological study of professional pesticide applicators that opened doors for epidemiological PD research. A few other case studies were presented, and the talk also introduced what would be an important player in this session, TCE (or trichloroethylene), which is a source of occupational solvent exposure in PD and has been a common exposure since the 1920s. TCE is found in degreasing metal parts and was previously found as a drycleaning solvent and a surgical anesthetic until 1977. Overall, this talk suggested moving toward individual risk modeling and that early life exposures are important. Exposures are hard and slow to model in humans, but as a field, we want to move toward prevention and intervention, risk reduction, diet, exercise, and pharmaceuticals.
The next couple of talks introduced some new PD concepts, such as exposomics, starting with Gary Miller of Emory University. Exposomics is a relatively new field, and the term exposome was coined in 2005. It is a hot topic in the field, and Dr. Miller provided insights into this field. Then, Briana De Miranda of University of Alabama at Birmingham spoke about TCE as an important toxicant of research in the field right now. Although it has a decreasing use over time, much of the TCE that has been admitted in the past several decades is still in the environment. The majority of TCE risk comes from vapor intrusion, and it is epidemiologically linked to PD. This talk featured information on whether or not route of exposure matters with TCE and also featured some highlights on lyposomal dysfunction in PD.
The order of the session got switched up due to some technical difficulties, so next was Andrew Koemeter-Cox from the Michael J. Fox Foundation. This talk detailed the foundation’s efforts to combat PD. The foundation was founded in 2000 by Michael J Fox and has funded more than 4,000 projects to date. Thirty-one percent of these projects are outside the US. Dr. Koemeter-Cox noted that the focus of PD research has been tied to genetic risk, but only 25% of PD cases can be tied to genetics, so the environment must be considered a factor. One of the goals of the foundation is to identify and understand environmental triggers of PD, and to do this, collaboration is needed, as well as expertise from disease-relevant models. The foundation also focuses on funding research on underrepresented populations.
Finally, Alison Bernstein of Rutgers, The State University of New Jersey ended the session with her talk on dieldtrin exposure and PD. Dr. Berstein researches epigenetics as a central mediator for PD risk. Her lab focuses on DNA modifications. Dieldrin is a toxicant with which high serum levels are associated with increased risk of PD, and elevated levels have been found postmortem in the PD brain. Dieldrin disrupts PD-related proteins, causes oxidative stress, and damages the dopamine system in animal and cellular models. Exposure is mainly dietary, and it accumulates in fatty tissues. It was widely used in the from the 1950s to 1987, and although exposure to the general population has declined and new exposure is not a concern, people who were exposed are still alive and not quite old enough to have PD. In her lab, Dr. Berstein models dieldrin and PFF exposure in a two-hit model. She has found, notably, that at 12 weeks of age in a mouse model, dieldrin induces changes in neuroinflammation. She has also seen sex-specific effects on expression of neuroinflammatory genes. Dr. Berstein described dieldrin as a chemical of high concern.
Overall, I believe this session highlighted the importance of persistent environmental exposure. While we may not be at high risk for some chemicals in a new exposure scenario, there are many chemicals that persist in the environment and carry risk for disease. TCE and dieldrin are two of those chemicals, and this session highlighted the importance of studying them. Overall, PD is a hot topic in research right now, and this session gave a breadth of insight as to the state of the research field.
This blog reports on the Symposium Session titled “Accelerating Discovery in Parkinson’s Disease: A Blueprint for Modeling Environmentally Relevant Exposures through Cross-Disciplinary Collaboration” that was held during the 2024 SOT Annual Meeting and ToxExpo. An on-demand recording of this session is available for meeting registrants on the SOT Online Planner and SOT Event App.
This blog was prepared by an SOT Reporter and represents the views of the author. SOT Reporters are SOT members who volunteer to write about sessions and events in which they participate during the SOT Annual Meeting and ToxExpo. SOT does not propose or endorse any position by posting this article. If you are interested in participating in the SOT Reporter program in the future, please email SOT Headquarters.
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