How exposure to the solvent trichloroethylene may harm brain cell 'cleanup' systems and lead to Parkinson's
The role of lysosomal impairment in trichloroethylene induced Parkinsonian neurodegeneration
This project explores whether exposure to the common industrial solvent trichloroethylene damages the brain’s cellular 'recycling' system and contributes to Parkinson’s disease in adults.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Alabama at Birmingham NIH-funded |
| Lab location | 1 site (Birmingham, United States) |
| Project ID | NIH-11471402 on NIH RePORTER |
What this research studies
This research looks at how trichloroethylene (TCE), a widespread chlorinated solvent, might cause Parkinson-like damage by impairing the lysosome-based cleanup system in brain cells. The team uses laboratory cell models and adult rodents to track lysosomal function, LRRK2 kinase activity, and buildup of misfolded alpha-synuclein protein. Their experiments aim to show how environmental exposure and a known genetic risk factor converge on the same cellular pathway. Findings could help identify exposure markers or biological targets to protect neurons.
Who could benefit from this research
Good fit: Adults with Parkinson’s disease or people concerned about past occupational or environmental exposure to industrial solvents could be considered most relevant to this line of research.
Not a fit: People seeking an immediate treatment for Parkinson’s symptoms or those without any history of solvent exposure may not see direct or near-term benefit from this preclinical research.
Why it matters
Potential benefit: If confirmed, the work could point to ways to prevent or slow Parkinson’s by reducing harmful exposures or by targeting lysosomal function or LRRK2-related pathways.
How similar studies have performed: Previous lab and animal studies, including work from this group, have linked TCE exposure to lysosomal problems, alpha-synuclein accumulation, and dopaminergic neuron loss, but human therapies based on this mechanism are not yet established.
Where this research is happening
Birmingham, United States
- University of Alabama at Birmingham — Birmingham, United States (Active)
Researchers
- Principal investigator: De Miranda, Briana — University of Alabama at Birmingham
- Study coordinator: De Miranda, Briana
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.