Abstract
This Perspective outlines the challenges addressed at the first Annual Parkinson’s Disease (PD) Prevention Think Tank, held on November 20–21, 2025 in Gainesville, Florida at the Fixel Institute. Over the course of two days, attendees from a wide variety of disciplines, including movement disorders neurology, environmental sciences, agriculture, public policy, public health, patient advocate groups, and more, discussed the current state of primary prevention research in PD, examined the lessons learned from prevention research in other disorders, and identified necessary regulatory and policy actions for moving toward primary prevention of PD. Eight key components of primary prevention are identified (8 C’s): accurately Count incidence and prevalence, Conduct longitudinal cohort studies, induce policy Change, Counsel on individual behavior change, Communicate clearly with the general public and with key stakeholders, form multi-centric Coalitions across neurodegenerative disorders, apply Cross-disciplinary approaches, and provide sustained financial Commitment to support ongoing prevention and mitigation efforts. These proceedings serve as an initial call-to-action for at-risk individuals, the clinicians who care for them, and for policymakers.
Subject terms: Diseases, Health care, Neurology, Neuroscience
Introduction
Parkinson’s disease (PD) is the world’s fastest-growing neurodegenerative disorder1,2. In 2025, an estimated 1.1 M individuals in North America were living with PD, with approximately 90,000 new diagnoses every year, making PD the second-most common neurodegenerative disorder after Alzheimer’s disease3,4. In light of an aging population and in the absence of a definitive disease-modifying treatment, the incidence and prevalence of PD are likely to grow rapidly in coming decades2, with profound health and economic impacts at the individual, family, health system, and societal levels5–8. Thus, strategies to prevent PD are urgently needed. Prevention may be subdivided into three types9: primary prevention to impede initiation of the disease process, secondary prevention to slow its progression in early or prodromal stages of disease prior to a traditional diagnosis, and tertiary prevention to minimize subsequent disability or disease-related complications. Studies of secondary10 and tertiary prevention11 in PD are underway, however primary prevention has received relatively little attention to date.
On November 20–21, 2025, the Parkinson’s Foundation and the Fixel Institute at the University of Florida convened a think tank to outline the current state of prevention research in PD, to examine the lessons learned from prevention research in other disorders, and to inform future regulatory and policy actions for primary prevention of PD. Over the course of two days, expert attendees from multiple healthcare, research, and policy disciplines (Table 1) discussed the urgent need for prevention and mitigation strategies, the impact of effective science communication, and the use of new technologies to track symptomatology at the individual and population levels. Consensus was reached on seven key action items (summarized as the 8 C’s) in Fig. 1.
Table 1.
Think-Tank Attendees
| Name | Institution/Affiliation |
|---|---|
| Rhoda Au, PhD | Boston University |
| Kelly Balmant, PhD | University of Florida |
| Anastasia Barnes, MD | University of Florida |
| Cynthia Barnett | University of Florida |
| James Beck, PhD | Parkinson’s Foundation |
| Kathleen Blake MD, MPH | Parkinson’s Foundation Patient Advisory Council |
| Bas Bloem MD, PhD, FRCPE | Radboud Medical Centre |
| Evangelos Christou, PhD | University of Florida |
| Wendy Dahl, PhD, RD | University of Florida |
| Laura Dalton | Harvard University |
| Briana de Miranda,PhD | University of Alabama at Birmingham |
| Alessandro Di Rocco, MD | Northwell Health |
| Ray Dorsey, MD, MBA | Atria Health and Research Institute |
| Ruogu Fang, PhD | University of Florida |
| J. Daniel Fenn MD, PhD | University of Florida |
| John Michael Gaziano MD, MPH | Massachusetts General Hospital/ Brigham |
| Sue Goldie MD, MPH | Harvard University |
| Samuel M. Goldman MD, MPH | University of California San Francisco |
| Paulina Gonzalez-Latapi, MD, Msc | Northwestern University |
| Diego Guarin, PhD | University of Florida |
| Kayln Henkel | Parkinson’s Foundation |
| Jonathan Kalmuss-Katz | EarthJustice |
| Jeongim Kim PhD | University of Florida |
| Brittany Krzyzanowski PhD | Barrow Neurological Institute |
| John Lehr | Parkinson’s Foundation |
| Nicole Lessard, BA, RN | Parkinson’s Foundation |
| Andi Lipstein Fristedt | Parkinson’s Foundation |
| Sneha Mantri MD, MS, FAAN | Parkinson’s Foundation |
| A. Enrique Martinez Nunez MD | University of Florida |
| Tejas R Mehta, MD | University of Florida |
| Monica Norcini PharmD, PhD | Fresco Parkinson Institute Italia Onlus Foundation |
| Michael Okun, MD | University of Florida Health, Norman Fixel Institute for Neurological Diseases |
| Peggy Borum, PhD | University of Florida |
| Jennifer L. Purks MD | University of Florida Health, Norman Fixel Institute for Neurological Diseases |
| Dawn Schiehser,PhD | University of Florida |
| Michael A. Schwarzschild MD, PhD | Massachusetts General Hospital |
| Karla Shelnutt PhD, RD | University of Florida, Institute of Food and Agricultural Sciences |
| Caroline (Carlie) Tanner, MD, PhD | University of California - San Francisco |
| Alexis Temkin, PhD | Environmental Working Group |
| J. Bryan Unruh, PhD | University of Florida, Institute of Food and Agricultural Sciences |
| Chris Vulpe MD, PhD | University of Florida, Center for Environmental and Human Toxicology |
| Kristin Wallock, OTD, MS, OTR/L | Parkinson’s Foundation |
| Cordelia Walz | Parkinson’s Foundation |
| Allison Willis MD, MS | University of Pennsylvania |
| Basma Yacoubi, PhD | University of Florida |
Fig. 1. Multi-Pronged Approach and Calls-to-Action for Primary Prevention of Parkinson’s Disease.

Primary prevention of a chronic, complex disorder like Parkinson’s disease requires a multi-pronged approach that interlaces research (accurate counts, cohort studies, and cross-disciplinary strategy), policy initiatives (regulatory change, chemical bans, and sustained funding commitments at federal and state levels), individual decisions (behavior and lifestyle changes), and interpersonal engagement (coalition building, science communication).
Current State of Prevention Research in PD
The Think Tank opened with a presentation on the geospatial analysis of PD in the United States. By overlaying individual patient data from the national Medicare dataset with land-use data from community use surveys, spatial and temporal trends in PD incidence, particularly in areas exposed to pesticides and chemicals, can be potentially uncovered12. For instance, agricultural land-use is strongly associated with PD prevalence, with populations in certain regions experiencing almost double the odds of PD13. This increased risk is modulated by additional geographic factors such as wind speed or groundwater sources14, as well as by chemical factors such as volatilization or environmental persistence. The data on specific chemical classes, including organochlorines15, organophosphates16, and chlorinated solvents17, were reviewed in detail. Notably, these risks are associations rather than definitive evidence of causation, reflecting the inherent challenges of causal inference in environmental epidemiology18. Observational studies are subject to potential confounding, exposure misclassification, and the complexity of long latency periods and mixed exposures across the life course. Because randomized exposure studies are not feasible, causal inference relies on integrating evidence across epidemiologic, toxicologic, and mechanistic studies, as well as frameworks such as the Bradford Hill criteria19. Approaches such as triangulating evidence from multiple data sources can strengthen causal interpretation while still acknowledging the remaining uncertainty.
From here, the conversation turned to mitigation principles. These were further divided into individual mitigation strategies, such as the use of personal protective equipment when applying pesticides20 and the protective effect of a healthy diet21, compared to societal mitigation strategies, such as the discontinuation or cleanup of toxic substances22. Exposure to chemical substances via different environmental media (e.g., water, soil, air) and routes of exposure (e.g., ingestion, topical, inhalation) and across the life-course were discussed. The Think Tank noted the paucity of data on real-world mixtures of different compounds, as well as exposure conditions in the host (e.g., age, sex, microbiome) that might prime certain individuals to develop disease. These effects may be mediated through biologically plausible mechanisms23,24, such as mitochondrial dysfunction, neuroinflammation, α-synuclein–related pathology, and related cellular stress pathways as well as through epigenetic mechanisms25. The neurotoxic potential of paraquat26–28, chlorpyrifos29,30, and trichloroethylene/perchloroethylene17,31,32, are well-documented in animal and epidemiological models of PD. Ongoing real-world research on chemical mixtures and routes of administration would further strengthen causal inference between exposure and disease, particularly by improving exposure characterization and reducing uncertainty in observed associations.
Lessons Learned from Prevention Research in Other Disorders
Several analogies were made between PD and other disorders, including cancer, cardiac disease, and dementia. In each of these case examples, as in PD, the disease process begins years or decades before the onset of symptoms, providing both a challenge and an opportunity for prevention through improved screening processes, greater public awareness of individual risk, and more effective regulatory measures that can be employed to lower the risk of disease.
For instance, the link between cigarette smoke and lung cancer led to successful campaigns for smoking cessation (individual behavior change)33,34, smoking bans in many public areas, including schools, hospitals, and offices (organizational change), and the removal of some tobacco products from the market (regulatory change)35. These multi-pronged policy efforts ultimately led to a reduction in the incidence of lung cancer as well as a reduction in the risk of a second smoking-related condition, cardiovascular disease36. In contrast to current public awareness of the health risks of smoking, public awareness of PD remains relatively low37, suggesting a prime opportunity to improve effective science communication38 regarding both individual and community risk.
Considering the complexity of PD risk patterns, which are likely influenced by genetics as well as lifestyle, Think Tank participants emphasized the importance of multimodal data collection to enable triangulation of data points. For instance, genetic studies may be combined with fluid biomarkers, digital phenotypes, individual behaviors, and clinical correlates to provide a comprehensive understanding of the disease state and disease complexity. Specific examples from the Million Veteran Program39 and the Framingham Heart Study40 were discussed in detail. The possibility of using artificial intelligence and machine learning algorithms for early identification41–44, remote monitoring of disease progression45, and drug discovery46,47 were discussed as an important vehicle for multimodal data collection.
Recommendations for Primary Prevention in PD
Think Tank participants reached consensus, leading to 8 key recommendations (8 C’s) to drive change in primary PD prevention (Fig. 1). These recommendations span all levels of the socioecological model of health promotion48 and bridge individual, interpersonal, research, and policy platforms.
Counts of disease prevalence and incidence to examine secular trends
Epidemiological studies1,2 have revealed that both incidence and prevalence of PD are rising worldwide at a rate too high to be accounted for by the mere aging of the population or the impact of genetic factors alone. Our understanding of secular trends in PD epidemiology relies on consistent and accurate counts of disease. Administrative claims data, door-to-door community surveys, and clinical registries all have challenges and benefits. However, in the absence of accurate, precise, and consistent measures of disease burden, it will be impossible to determine the true impact of any prevention strategy. For instance, the creation of a PD registry, database, or cohort would allow insight into the impact of any given intervention. When policy changes are implemented in specific regions, it may be equally valuable to track incidence in surrounding or otherwise similar regions, which may serve as contemporary controls.
Cohorts with deep phenotyping to integrate genetics, clinical, exposure, and digital data
The heterogeneity of PD may prove to be both an advantage and a challenge for prevention. It is likely PD has multiple upstream causes, and the interplay between them may prove challenging to untangle. Nevertheless, the need for well-phenotyped, diverse cohorts that integrate multiple data sources is clear. By combining genetic, clinical, digital, and exposure data, we will gain a greater understanding of gene-environment interactions and of the mechanistic complexity of disease processes, which may provide further insights into disease-modifying therapies.
Changes in policy and regulation
Improved understanding of gene-environment interaction and disease mechanism can inform the policy and regulatory changes that are urgently needed to reduce exposure to neuro-toxicants. The U.S. Environmental Protection Agency (EPA) and other equivalent agencies around the world should take regulatory action to protect people from toxic chemicals linked to PD, such as paraquat, chlorpyrifos, trichloroethylene, and perchloroethylene. Where sufficient scientific data demonstrating these pesticides pose an unreasonable risk already exists, the EPA should initiate pesticide registration cancellation. And as new research about health and environmental exposure risks emerges, EPA should review evidence without delay to determine if the “reasonable certainty of no harm” standard has been violated or if the proposed uses lead to unreasonable risk. In the U.S., individual states can act to stop or stem exposure to chemicals; multiple states are already taking steps in this direction.
Counseling around individual behavior change
Individual behavior changes, such as greater use of protective equipment, improved hygiene practices, and other strategies, could decrease an individual’s exposure risk to neurotoxic agents. Lifestyle changes, such as exercise and diet, are associated with a lower risk of PD21,49–51. Those with known genetic risks, strong family history of PD, or even prodromal features may be particularly motivated to make these changes. Given the long lead time between exposure and disease, however, some may not feel a pressing urgency to make lifestyle changes. In addition, given the broad set of factors that influence exposure (e.g., agricultural and industrial land-use patterns, occupational practices and worker protections, socioeconomic and environmental inequities) risk reduction will not be possible for many individuals. Finally, given the nature of environmental contamination of air, water, and soil, passive exposure to toxicants will remain a risk. This reality underscores the essential need for multi-layered intervention.
Communication to educate the public and policymakers
Even though PD is the fastest-growing neurodegenerative condition worldwide and the second most common neurodegenerative condition in North America, public awareness of PD remains low37. Principles of effective science education and communication, such as clear and consistent messaging, tailored to audience needs, and infused with a call-to-action, should be adopted by researchers, clinicians, and policymakers.
Coalition-formation across disease entities
The similarities between PD and other synucleinopathies, or PD and other neurodegenerative disorders, should be leveraged to achieve greater synergy. Changes at the individual, community, and national level that are beneficial for one disorder may have beneficial effects for another. Strong coalitions across multiple disease entities, such as the Neuro-Impact Coalition52 have the potential to attract attention that may reach beyond any individual disorder.
Cross-disciplinary research and strategy
Think Tank attendees recognized that cross-disciplinary research and strategy need to be a top priority for PD prevention. To drive change on both an individual and a systems level, multiple stakeholder groups are needed. For instance, behavioral psychologists may provide greater insight into decision-making processes and tradeoffs for individuals. Health economists can provide data on the disease-related financial and non-financial burdens borne by families and communities. Molecular biologists and toxicologists can provide a mechanistic understanding of disease progression. The voices of people with PD were represented at the Think Tank and will continue to be critical to this work. As with other coalitions, a multi-disciplinary, multi-pronged approach is likely to yield the greatest benefit and impact for PD prevention.
Commitment to fund research and mitigation
Research into PD prevention and mitigation will be critically important. Despite rising disease burden and rising cost of care, federally funded research in PD has remained flat since FY2021; when adjusted for inflation, this represents a decrease of approximately 20%. Disease-specific foundations are endeavoring to bridge the gap by providing additional funding for research and innovation, and some states are considering their own research investments. However, in the U.S., without a sustainable federal funding strategy, early-stage research may never reach the communities at greatest risk. As a starting point, the Parkinson’s community is advocating for $600 million dedicated for PD research by the NIH on an annual basis by 2028.
Conclusion
Two hundred years after James Parkinson initially described PD, both global incidence and prevalence of the disease are rapidly rising. This rate of change suggests that environmental exposures and/or lifestyle factors may be contributing to the development of manifest motor PD, combined for some with an underlying genetic susceptibility. Such exposures may be active (e.g., spraying pesticides, ingesting dopamine-blocking or dopamine-toxic agents); others may be passive (e.g., volatilization of toxicants with distant spread, contamination of groundwater or other sources). Continued inaction will likely result in increasing rates of disability and premature death from PD, with profound economic consequences. We urge the Parkinson’s community in the U.S. and globally to consider the eight components (C’s) of primary prevention: accurate Counts of disease burden, longitudinal Cohort studies, policy Change, individual Counseling, science Communication, disease Coalitions, Cross-disciplinary approaches, sustained financial Commitment.
Acknowledgements
The authors wish to thank Kelly Balmant, Cynthia Barnett, Bas Bloem, Laura Dalton, Alessandro di Rocco, John Michael Gaziano, Jonathan Kalmuss-Katz, Jeongim Kim, A. Enrique Martinez-Nunez, Karla Shelnutt, and Basma Yacoubi for their participation in the Think Tank. No funding was received for this work.
Author contributions
S.M. and M.S.O. wrote the main manuscript text. S.M. prepared Figure 1 and Table 1. All authors (S.M., R.A., A.B., J.B., K.B., W.D., Bd.M., E.R.D., R.F., J.D.F., S.J.G., S.M.G., P.G.-L., D.G., B.K., N.L., A.L.F., T.R.M., M.C., P.B., J.L.P., D.S., M.A.S., C.M.T., A.T., A.W.W., J.B.U., C.V., K.W., C.W., M.S.O.) reviewed the manuscript.
Data availability
No datasets were generated or analysed during the current study.
Competing interests
R.A. is a Scientific advisor to Signant Health & NovoNordisk. B.dM. is a Guest Editor for a Special Collection in npj Parkinson’s disease on “Environmental risk factors for Parkinson’s disease”; she was not involved in the journal’s review of, nor decisions related to, this manuscript. B.dM. reports grant funding from NIEHS, APDA, US DoD, and Parkinson’s Foundation; consulting fees from The Miller Firm and Bell Legal Group; payment for expert testimony from the US DoJ related to Camp Lejeune litigation; support for attending meetings from Parkinson’s Foundation, The Michael J. Fox Foundation for Parkinson’s Research, the University of Georgia, the World Federation of Neurology; participation in a DSMB or SAB for the APDA and MJFF. ERD reports honoraria from Adivo Associates France, American Neurological Association, Dartmouth, Elsevier, HMP Education, International Parkinson and Movement Disorder Society, Massachusetts Medical Society, Michael J. Fox Foundation, National Institutes of Health, National Multiple Sclerosis Society, Northwestern University, Patient-Centered Outcomes Research Institute, Philadelphia Neurological Society, Stanford University, Stony Brook, Sutter Health, Texas Neurological Society, University of Toronto; consulting fees from Abbott, Abbvie, Acadia, Acorda Therapeutics, Advarra, Aspen Neuroscience, Inc., Bial Pharmaceuticals, Biogen, Biohaven Pharmaceuticals, BioSensics, Boehringer Ingelheim, Caraway Therapeutics, Cerevance, CuraSen, DConsult2, Denali Therapeutics, Eli Lilly, Genentech, HanAll BioPharma, Health & Wellness Partners, HMP Education, Kairos Cinema, LLC (PBS), Karger, KOL groups, Life Sciences Consultant, Mediflix, Medrhythms, Merck, Mitsubishi Tanabe Pharma America, Inc., MJH Holdings, NACCME, Novartis, Otsuka, Praxis Medicine, Remepy, Sanofi, Seelos Therapeutics, Spark Therapeutics, Springer Healthcare, Synucure Therapeutics, Theravance Biopharmaceuticals, Vima Therapeutics, VivoSense, WebMD; grants from Averitas Pharma, Biogen, Burroughs Wellcome Fund, Michael J. Fox Foundation, National Institutes of Health, Pfizer, Photopharmics, Roche, Safra Foundation; ownership interests in Included Health, Mediflix, SemCap, Synapticure; patents with the Chorea Index. S.M.G. reports grant support from Michael J. Fox Foundation, US National Institutes of Health, US Department of Defense, US Veterans Administration; consulting fees from Michael J. Fox Foundation and Alkahest. P.G.-L. reports grant support from the Parkinson’s Foundation and the Michael J. Fox Foundation. CMT declares consultancies for Praxis (advisory board via the International Parkinson’s and Movement Disorder Society), Jazz/Cavion, and Roche Genentech. She declares data monitoring committee service for Bial and Hillhurst. C.M.T. also declares grant support to her institution from The Michael J. Fox Foundation, National Institutes of Health, Gateway LLC, Department of Defense, Roche Genentech, and Parkinson Foundation. A.T. is an employee of the Environmental Working Group, a nonprofit research and advocacy organization. A.T. declares no personal financial conflict of interest. Within the scope of their employment, A.T. has prepared written and oral comments on behalf of EWG to the U.S. Environmental Protection Agency, as well as state and local agencies regarding regulation of pesticides as well as drinking water quality. As an organization, EWG evaluates and publicly comments on health impacts of drinking water contaminants in a publicly viewable database of drinking water contaminants (https://www.ewg.org/tapwater/). EWG also licenses, for a fee, the data in this database to other organizations, including water filter companies, in furtherance of our work. A.W.W. receives funding from the the National Instituties of Health. J.B., N.L., A.L.F., S.M., K.W., and C.W. are employees of the Parkinson’s Foundation. The remaining authors report no relevant disclosures related to the current manuscript.
Footnotes
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Dorsey, E. R. et al. Global, regional, and national burden of Parkinson’s disease, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol.17, 939–953 (2018). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Su, D. et al. Projections for prevalence of Parkinson’s disease and its driving factors in 195 countries and territories to 2050: modelling study of Global Burden of Disease Study 2021. BMJ388, e080952 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Pearson, C. et al. Care access and utilization among medicare beneficiaries living with Parkinson’s disease. NPJ Parkinsons Dis.9, 108 (2023). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Willis, A. W. et al. Incidence of Parkinson disease in North America. npj Parkinsons Dis.8, 1–7 (2022). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Albarmawi, H. et al. The economic burden of Parkinson disease among Medicare beneficiaries. J. Manag Care Spec. Pharm.28, 405–414 (2022). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Wijers, A., Ravi, A., Evers, S. M. A. A., Tissingh, G. & van Mastrigt, G. A. P. G. Systematic Review of the Cost of Illness of Parkinson’s Disease from a Societal Perspective. Mov. Disord.39, 1938–1951 (2024). [DOI] [PubMed] [Google Scholar]
- 7.Yang, W. et al. Current and projected future economic burden of Parkinson’s disease in the U. S. npj Parkinsons Dis.6, 1–9 (2020). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Mantri, S., Fullard, M. E., Beck, J. & Willis, A. W. State-level prevalence, health service use, and spending vary widely among Medicare beneficiaries with Parkinson disease. npj Parkinsons Dis.5, 1 (2019). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.McKenzie, J. F. & Seabert, D. M. Prevention: Primary, Secondary, and Tertiary. in Encyclopedia of Epidemiology 839–840 (SAGE Publications, Inc., 2008). 10.4135/9781412953948. [DOI]
- 10.Crotty, G. F., Ayer, S. J. & Schwarzschild, M. A. Designing the first trials for Parkinson’s prevention. J. Parkinsons Dis.14, S381–S393 (2024). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Tanner, C. M. et al. The TOPAZ study: a home-based trial of zoledronic acid to prevent fractures in neurodegenerative Parkinsonism. npj Parkinsons Dis.7, 16 (2021). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Young, S. G., Elwell, K. & Watts, C. R. Regional changes in the prevalence of Parkinson’s disease over a ten-year period in the state of Texas. Clin. Park Relat. Disord.13, 100369 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Krzyzanowski, B., Beyene, K. M., Nielsen, S. S., Killion, J. A. & Racette, B. A. Cropland associated with risk of Parkinson’s disease in the northern Great Plains. Parkinsonism Relat. Disord.132, 107288 (2025). [DOI] [PubMed] [Google Scholar]
- 14.Silver, M. R., Racette, B. A., Dube, U., Faust, I. M. & Searles Nielsen, S. Well Water and Parkinson’s Disease in Medicare Beneficiaries: A Nationwide Case-Control Study. J. Parkinsons Dis.10, 693–705 (2020). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Xu, Y., Su, Y., Cai, S., Yao, Y. & Chen, X. Environmental and occupational exposure to organochlorine pesticides associated with Parkinson’s disease risk: a systematic review and meta-analysis based on epidemiological evidence. Public Health237, 374–386 (2024). [DOI] [PubMed] [Google Scholar]
- 16.Chen, Y. et al. Mechanisms of neurotoxicity of organophosphate pesticides and their relation to neurological disorders. Neuropsychiatr. Dis. Treat.20, 2237–2254 (2024). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Krzyzanowski, B., Beyene, K. M., Turner, J. R. & Racette, B. A. Ambient trichloroethylene exposure and parkinson disease risk in medicare beneficiaries. Neurology105, e214174 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Pearce, N., Vandenbroucke, J. & Lawlor, D. A. Causal inference in environmental epidemiology: old and new. Epidemiology30, 311–316 (2019). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Shimonovich, M., Pearce, A., Thomson, H., Keyes, K. & Katikireddi, S. V. Assessing causality in epidemiology: revisiting Bradford Hill to incorporate developments in causal thinking. Eur. J. Epidemiol.36, 873–887 (2021). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Furlong, M. et al. Protective glove use and hygiene habits modify the associations of specific pesticides with Parkinson’s disease. Environ. Int75, 144–150 (2015). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Kamel, F. et al. Dietary fat intake, pesticide use, and Parkinson’s disease. Parkinsonism Relat. Disord.20, 82–87 (2014). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Fagundes, T. R., Coradi, C., Vacario, B. G. L., de Morais Valentim, J. M. B. & Panis, C. Global evidence on monitoring human pesticide exposure. J. Xenobiot.15, 187 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Amaral, L. et al. The neurotoxicity of pesticides: Implications for Parkinson’s disease. Chemosphere377, 144348 (2025). [DOI] [PubMed] [Google Scholar]
- 24.Zhang, X.-F., Thompson, M. & Xu, Y.-H. Multifactorial theory applied to the neurotoxicity of paraquat and paraquat-induced mechanisms of developing Parkinson’s disease. Lab Invest96, 496–507 (2016). [DOI] [PubMed] [Google Scholar]
- 25.Singh, H., Kumari, S. & Taliyan, R. Epigenetic mechanisms linking environmental exposure to Parkinson’s disease: A comprehensive review. Neuroscience585, 367–380 (2025). [DOI] [PubMed] [Google Scholar]
- 26.Bosak, F. et al. Evaluation of the protective effects of noscapine on paraquat-induced Parkinson’s disease in rats. Mol. Neurobiol.62, 11848–11876 (2025). [DOI] [PubMed] [Google Scholar]
- 27.Kachroo, A., Irizarry, M. C. & Schwarzschild, M. A. Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration. Exp. Neurol.223, 657–661 (2010). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Shalikar, S., Mashayekhpour, M. A., Ebrahimi Vosta-Kalaee, S., Abouhosseini Tabari, M. & Hajizadeh Moghaddam, A. Frankincense improves motor symptoms and attenuates the progression of Paraquat (PQ)-induced Parkinson’s disease in mice by attenuating oxidative stress, inflammation, and apoptotic cell death and improving nerve growth factor gene expression. IBRO Neurosci. Rep.20, 276–285 (2026). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Hasan, K. M. M. et al. The pesticide chlorpyrifos increases the risk of Parkinson’s disease. Mol. Neurodegener.21, 3 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Zwartsen, A. et al. Towards NAM-based risk assessment for developmental neurotoxic effects, illustrated with chlorpyrifos. ALTEX 10.14573/altex.2412051 (2025). [DOI] [PubMed] [Google Scholar]
- 31.Liu, R., Zhang, F., Lou, J. & Song, F. Trichloroethylene exposure and Parkinson’s disease: environmental risk, metabolic pathways, and mechanistic insights. Mol. Neurobiol.62, 15336–15348 (2025). [DOI] [PubMed] [Google Scholar]
- 32.De Miranda, B. R. & Greenamyre, J. T. Trichloroethylene, a ubiquitous environmental contaminant in the risk for Parkinson’s disease. Environ. Sci. Process Impacts22, 543–554 (2020). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Corelli, R. L. & Hudmon, K. S. Pharmacologic interventions for smoking cessation. Crit. Care Nurs. Clin. North Am.18, 39–51, xii (2006). [DOI] [PubMed] [Google Scholar]
- 34.Nian, T. et al. Non-pharmacological interventions for smoking cessation: analysis of systematic reviews and meta-analyses. BMC Med21, 378 (2023). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Deyton, L., Sharfstein, J. & Hamburg, M. Tobacco Product Regulation — A Public Health Approach. N. Engl. J. Med.362, 1753–1756 (2010). [DOI] [PubMed] [Google Scholar]
- 36.Chang, J. T., Anic, G. M., Rostron, B. L., Tanwar, M. & Chang, C. M. Cigarette Smoking Reduction and Health Risks: A Systematic Review and Meta-analysis. Nicotine Tob. Res23, 635–642 (2021). [DOI] [PubMed] [Google Scholar]
- 37.Pan, S., Stutzbach, J., Reichwein, S., Lee, B. K. & Dahodwala, N. Knowledge and attitudes about Parkinson’s disease among a diverse group of older adults. J. Cross Cult. Gerontol.29, 339–352 (2014). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Borowiec, B. G. Ten simple rules for scientists engaging in science communication. PLoS Comput Biol.19, e1011251 (2023). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Pankratz, N., Cole, B. R., Beutel, K. M., Liao, K. P. & Ashe, J. Parkinson disease genetics extended to African and hispanic ancestries in the VA Million Veteran Program. Neurol. Genet10, e200110 (2024). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.O’Shea, S. et al. Obesity and the development of Parkinson’s disease within the Framingham Heart Study cohort. Clin. Park Relat. Disord.12, 100291 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Dennis, A.-G. P. & Strafella, A. P. The role of AI and machine learning in the diagnosis of Parkinson’s disease and atypical Parkinsonisms. Parkinsonism Relat. Disord.126, 106986 (2024). [DOI] [PubMed] [Google Scholar]
- 42.Reddy, A. et al. Artificial intelligence in Parkinson’s disease: Early detection and diagnostic advancements. Ageing Res Rev.99, 102410 (2024). [DOI] [PubMed] [Google Scholar]
- 43.Guarín, D. L. et al. Video analysis reveals early signs of Bradykinesia in REM sleep behavior disorder and Parkinson’s disease. NPJ Parkinsons Dis.11, 222 (2025). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44.Guarín, D. L., Wong, J. K., McFarland, N. R., Ramirez-Zamora, A. & Vaillancourt, D. E. What the trained eye cannot see: Quantitative kinematics and machine learning detect movement deficits in early-stage Parkinson’s disease from videos. Parkinsonism Relat. Disord.127, 107104 (2024). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Little, M. A. Smartphones for remote symptom monitoring of Parkinson’s Disease. J. Parkinsons Dis.11, S49–S53 (2021). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46.Karimi-Sani, I. et al. Drug repositioning for Parkinson’s disease: an emphasis on artificial intelligence approaches. Ageing Res Rev.104, 102651 (2025). [DOI] [PubMed] [Google Scholar]
- 47.Vatansever, S. et al. Artificial intelligence and machine learning-aided drug discovery in central nervous system diseases: state-of-the-arts and future directions. Med Res Rev.41, 1427–1473 (2021). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 48.Golden, S. D. & Earp, J. A. L. Social ecological approaches to individuals and their contexts: twenty years of health education & behavior health promotion interventions. Health Educ. Behav.39, 364–372 (2012). [DOI] [PubMed] [Google Scholar]
- 49.Grazina, R. & Massano, J. Physical exercise and Parkinson’s disease: influence on symptoms, disease course and prevention. Rev. Neurosci.24, 139–152 (2013). [DOI] [PubMed] [Google Scholar]
- 50.Thornton, J. S. et al. Physical activity prescription: a critical opportunity to address a modifiable risk factor for the prevention and management of chronic disease: a position statement by the Canadian Academy of Sport and Exercise Medicine: Table 1. Br. J. Sports Med.50, 1109–1114 (2016). [DOI] [PubMed] [Google Scholar]
- 51.Gao, X. et al. Prospective study of dietary pattern and risk of Parkinson disease. Am. J. Clin. Nutr.86, 1486–1494 (2007). [DOI] [PMC free article] [PubMed] [Google Scholar]
- 52.Kopil, C. M. et al. A Coalition to Advance Treatments for Parkinson’s Disease, Dementia with Lewy Bodies, and Related Disorders. J. Parkinsons Dis.14, 1105–1114 (2024). [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
No datasets were generated or analysed during the current study.
