Virus Infection Causes Parkinson-Like Brain Damage in Mice, Offering New Disease Model

A recent investigation demonstrates that an everyday virus is capable of producing brain damage and movement impairments reminiscent of Parkinson’s disease.

Researchers typically rely on animal models that simulate Parkinson’s by employing genetic alterations or exposing subjects to neurotoxic chemicals. While these approaches replicate many disease features, they may fall short of capturing how the disorder emerges naturally in humans.

Now, a team at Texas A&M University has introduced a non‑toxic strategy that induces Parkinson‑like symptoms by infecting mice with Theiler’s murine encephalomyelitis virus (TMEV), a virus that naturally occurs in rodent populations.

This breakthrough shows that a straightforward viral infection can generate the same neuronal loss and motor deficits observed in human Parkinson’s patients, opening new avenues for research.

“Models that depend on toxic exposure are valuable, but not every individual exposed to chemicals develops Parkinson’s, so those models cannot reflect all the ways a complex disease like Parkinson’s may begin or progress in people,” explains Candice Brinkmeyer‑Langford, a neurodegenerative‑disease specialist at Texas A&M’s School of Public Health.

Parkinson’s disease affects more than 10 million people worldwide, making it the second most common brain disorder after dementia. The condition destroys dopamine‑producing neurons, leading to balance problems, slowed walking, hand tremors, rigidity, and often mental or emotional challenges.

Although the precise triggers remain unknown, scientists have long suspected that viral‑induced brain inflammation—potentially from infections acquired decades earlier—combined with genetic and environmental factors could initiate the disease. Brinkmeyer‑Langford and colleagues previously highlighted a similar viral link in amyotrophic lateral sclerosis (ALS).

“Viruses can provoke very different illnesses depending on a person’s genetic makeup,” she notes. “For instance, Epstein‑Barr virus causes mononucleosis but may also contribute to cancer or multiple sclerosis, and SARS‑CoV‑2 can affect the heart, brain, and lungs.”

To assess whether TMEV serves as a reliable Parkinson’s model, the researchers measured three key outcomes:

• Neuronal infection and loss. One week after exposure, the team confirmed that TMEV had entered dopamine‑producing cells. By the fourth week, those cells were markedly depleted at the infection site. When a dopamine‑mimicking drug was administered, infected mice (n = 13) displayed movement patterns distinct from healthy controls (n = 14), confirming progressive loss of dopamine neurons.
• Motor speed and coordination. Using the pole test, the investigators compared the ability of infected versus control mice to navigate a vertical pole. Infected animals required more time to complete the task, a deficit that persisted through the study’s 20‑week endpoint.
• Walking dynamics. A specialized treadmill recorded over 100 parameters related to gait, balance, and motor function. Results showed that TMEV‑infected mice exhibited reduced walking efficiency, mirroring the weakness that follows dopamine‑cell loss in Parkinson’s patients.

Having validated this novel model, Brinkmeyer‑Langford anticipates future experiments that will directly contrast the TMEV system with traditional Parkinson’s models, seek early biomarkers, and explore how the immune response to viral infection reshapes the brain.

“The clock is ticking, since the rapidly aging global population means the number of people with Parkinson’s is expected to jump significantly,” she adds.

Funding was provided by the National Institute for Neurological Disorders and Stroke and a Texas A&M College of Veterinary Medicine and Biomedical Sciences Graduate Trainee Grant.