The Pest-PD study (NCT06420310) is a case-control cross-sectional prevalence study conducted by Hospital Universitario de Burgos in Spain. The study aims to determine whether individuals exposed to pesticides have a higher prevalence of preclinical and prodromal Parkinson's disease compared to unexposed controls. This is an epidemiological study investigating the environmental etiology of Parkinson's disease through the lens of pesticide exposure as a major modifiable risk factor.
Unlike interventional clinical trials, Pest-PD is an observational study that will assess biomarker and clinical sign prevalence in pesticide-exposed vs. unexposed populations. The mechanistic focus aligns with the broader literature implicating pesticide exposure as a dominant environmental driver of Parkinson's disease risk[1][2].
| Attribute | Value |
|---|---|
| NCT Number | NCT06420310 |
| Acronym | Pest-PD |
| Official Title | Prevalence of Preclinical and Prodromal Parkinson Disease in Subjects Exposed to Pesticides |
| Study Type | Observational (Case-Control) |
| Overall Status | Recruiting |
| Study Start Date | April 2024 |
| Estimated Primary Completion | September 2028 |
| Estimated Study Completion | December 2028 |
| Target Duration | 3 Years |
| Enrollment | 260 (estimated) |
| Condition | Pesticide-Induced Parkinsonism |
| Biospecimens | Blood samples with DNA |
| Data Sharing | No IPD sharing |
Epidemiological evidence has consistently demonstrated that pesticide exposure significantly increases Parkinson's disease risk. Key mechanistic pathways include:
MPTP-like compounds: The landmark 1983 Langston study established that compounds structurally similar to meperidine (MPTP) can induce parkinsonism in humans, directly linking pesticide-like molecules to dopaminergic neurodegeneration.
Rotenone and paraquat: Chronic systemic exposure to rotenone and paraquat in animal models reproduces the full spectrum of Parkinson's disease features, including mitochondrial complex I dysfunction, alpha-synuclein aggregation, and selective dopaminergic neuron loss[3].
Epigenetic mechanisms: Pesticides modify the expression of genes related to Parkinson's disease through epigenetic mechanisms, particularly affecting mitochondrial function and protein quality control pathways[4].
Gene-environment interaction: Genetic modifiers of Parkinson's disease risk significantly influence individual susceptibility to pesticide-induced neurodegeneration[5].
The study focuses on detecting prodromal Parkinson's disease — the pre-diagnostic phase characterized by non-motor symptoms that precede motor diagnosis by years to decades. Key prodromal markers include:
Pest-PD Study Design
├── Cases: Farmers with occupational pesticide exposure
│ └── N ≈ 130 individuals
└── Controls: Un-exposed individuals
└── N ≈ 130 individuals
The study collects blood samples from both cases and controls, including DNA for genomic analysis. This biospecimen collection enables:
| Measure | Description | Time Frame |
|---|---|---|
| Prodromal PD prevalence | Presence of early non-motor symptoms associated with preclinical/prodromal Parkinson's disease | Over the last year |
The study will compare:
| Facility | City | Country | Status |
|---|---|---|---|
| Hospital Universitario de Burgos | Burgos | Spain | Recruiting |
Esther Cubo, MD, PhD
Hospital Universitario de Burgos
Contact: +34 947 256 533 | mcubo@saludcastillayleon.es
The Pest-PD study directly supports the environmental etiology section of Environmental Toxins and Parkinson's Disease Risk. Key mechanistic connections:
This trial page provides anchor points for:
The Pest-PD study complements several other research streams in the NeuroWiki knowledge base:
Hospital Universitario de Burgos serves as the lead sponsor and coordinating center. The study represents a collaborative effort between neurology, epidemiology, and occupational medicine specialists in Spain.
Tang M, et al. Environmental toxicants as dominant cause of Parkinson's disease. Environ Health Perspect. 2024. ↩︎ ↩︎
Ball N, Stokes R, Chen H, et al. Parkinson's disease and environmental exposures. J Neurol Neurosurg Psychiatry. 2019. ↩︎
Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT. Chronic systemic pesticide exposure reproduces features of Parkinson's disease. Nat Neurosci. 2000. ↩︎ ↩︎
Aschner M, Neal AP, Pajarillo E, et al. Mitochondrial dysfunction and protein mishandling as shared mechanisms in multiple neurodegenerative diseases. Mol Brain. 2021. ↩︎
Hernandez DG, Reed X, Singleton AB. Genetic modifiers of Parkinson's disease risk associated with environmental exposures. NPJ Parkinsons Dis. 2023. ↩︎