Scientists typically use animal models when studying Parkinson’s disease. This is because these models mimic the disease well. However, the method has limitations because it requires genetic modification and injection of toxins, and may not accurately represent how the disease develops in humans.
But now researchers at Texas A&M University have developed a model that uses a non-toxic method to induce Parkinson’s symptoms: infection with a virus called Tyler Mouse Encephalomyelitis Virus (TMEV), a natural pathogen in mice.
Their work is game-changing because it demonstrates that a simple viral infection can cause the exact brain damage and disability seen in Parkinson’s disease patients in animal models, paving the way for further research.
Toxic exposure models are useful for studying Parkinson’s disease, but not all people exposed to chemicals will develop Parkinson’s disease, so these models cannot fully describe how a complex disease like Parkinson’s disease actually develops in humans or over time. ”
Candace Brinkmeyer Langford, Neurodegenerative Disease Specialist, Texas A&M University Texas A&M Health School of Public Health
Parkinson’s disease affects more than 10 million people worldwide and is the second most common brain disease after dementia. It destroys the cells that produce dopamine, a chemical essential for smooth body movement, causing balance and gait problems, trembling in the hands and fingers, general stiffness, and even mental or emotional distress.
Its origins are unknown, but experts have believed for decades that the disease may be caused by a combination of brain inflammation caused by a virus (even one infected decades ago), a person’s genetics and environmental factors. This idea was recently confirmed by Brinkmeyer-Langford and colleagues at Texas A&M in the case of amyotrophic lateral sclerosis (ALS), another devastating motor neuron disease.
“Viruses are known to cause completely different diseases based on a person’s genetics,” she says. “For example, Epstein-Barr virus causes mononucleosis, but it can also cause cancer and multiple sclerosis, and SARS-CoV-2 can attack not only the lungs but also the heart and brain.”
In this pilot study to test the effectiveness of TMEV in Parkinson’s disease research, researchers conducted experiments to measure:
- Infection and damage to brain cells. A week after infection, researchers confirmed that the virus had infected brain cells that produce dopamine. One month after infection, the dopamine-producing cells at the site of the virus infection were destroyed. Comparison of dopamine-induced behavior between 13 infected and 14 healthy control animal models after administration of dopamine mimetics resulted in distinct motor patterns confirming the loss of dopamine neurons. This test confirmed that the virus causes significant loss of these important dopamine brain cells over time.
- speed and coordination. They compared 13 infected animal models with 14 healthy control animal models, tracked and measured motor performance with a standard assessment called the pole test, and determined whether the loss of dopamine-producing cells causes the physical movement problems typically seen in Parkinson’s disease patients. The TMEV-infected animal model was slower to complete testing compared to the healthy control model, even at week 20, when the study ended.
- Abnormal gait. They analyzed how fast and efficiently the animal models walked using a specialized treadmill that assessed more than 100 factors involved in gait, motor function, and balance. The test confirmed that the virus causes physical weakness after the loss of dopamine-producing cells due to viral infection, and proved that the virus damaged the brain in a manner similar to that seen in patients with Parkinson’s disease.
With this innovative model now proven, Professor Brinkmeyer-Langford said future research will include directly testing the TMEV model against standard older animal models used in Parkinson’s disease research, looking for early warning signs and biological markers of Parkinson’s disease, and analyzing how the body’s immune response to the virus causes changes in the brain.
“The clock is ticking, as the number of people with Parkinson’s disease is expected to increase significantly due to the rapid aging of the world’s population,” she said.
Other researchers involved in the study, all from Texas A&M, included Tae Wook Kang, a graduate student in the College of Veterinary Medicine and Biomedical Sciences (VMBS), Rahul Srinivasan of the Naresh K. Vashisht School of Medicine, and C. Jane Welsh of VMBS and the Department of Neuroscience and Experimental Therapeutics. They are also affiliated with the Texas A&M Neuroscience Institute.
This research Brain, Behavior, Immunity – Health This research was supported by the National Institute of Neurological Disorders and Stroke and the Texas A&M College of Veterinary Medicine and Biomedical Sciences Graduate Trainee Grant.
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Reference magazines:
Kang, T.W.; others. (2026). Tyler murine encephalomyelitis virus as an infectious agent in a virus-induced mouse model of Parkinson’s disease. Brain, Behavior, Immunology – Health. DOI: 10.1016/j.bbih.2026.101230. https://www.sciencedirect.com/science/article/pii/S2666354626000633?via%3Dihub
