A Brain Virus May Trigger Parkinson’s in Some People and Scientists Are Starting to Take the Idea Seriously

Researchers link viral infection to Parkinson’s-like brain damage in mice.

A virus that normally infects mice has produced Parkinson’s-like brain damage in rodents without any other intervention.

In a pilot study, Texas A&M researchers used Theiler’s murine encephalomyelitis virus, or TMEV, to infect a small brain region that helps control movement. The infection destroyed dopamine-producing neurons at the site, disrupting walking and coordination. The result does not mean this particular virus causes Parkinson’s disease in people. It cannot because TMEV only affects rodents, but some other virus that can infect the human brain might.

Lasting Viral Damage in the Brain

Parkinson’s disease kills neurons that make dopamine. There are over 100 neurotransmitters in the human body, which are like tiny chemical mailmen that deliver messages between your nerve cells. Probably 99% are unknown to laypeople, but everybody knows about dopamine. Often erroneously called the pleasure molecule (a better moniker would be the ‘anticipation molecule’ because it floods your brain when you anticipate a reward, not when you receive it), dopamine is, in fact, also heavily involved in movement. Your brain needs this chemical to coordinate smooth movement.

As dopamine neurons disappear, people can develop tremors, stiffness, balance problems, changes in walking, and emotional distress. These symptoms are the hallmarks of Parkinson’s disease.

In order to study the disease in the lab, neuroscientists rely on Parkinson’s animal models. Typically, mice are given toxins or are genetically edited in order to produce the Parkinson’s symptoms. However, these attempts don’t always fully capture how Parkinson’s may begin in people.

“The toxic-exposure models are useful for studying Parkinson’s,” said Candice Brinkmeyer-Langford, a Texas A&M neurodegenerative disease researcher and one of the study’s authors. “But not all people who are exposed to chemicals go on to develop Parkinson’s, so these models cannot show all the ways a disease as complex as Parkinson’s actually begins or develops over time in people.”

In the study, researchers placed TMEV directly into the substantia nigra, a movement-control region deep in the mouse brain where dopamine-producing neurons are especially important. After one week, the virus had infected those neurons. After one month, the infection killed many of the neurons. The damage showed up in the animals’ bodies, too: infected mice moved more slowly, walked differently, and still showed motor problems 20 weeks after infection.

In one test, researchers placed mice at the top of a vertical pole and timed how long they took them to turn around and climb down. The infected mice were slower than the control mice, a sign that the virus had clearly affected coordination and movement control.

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The researchers also used tests that looked more closely at dopamine-related movement. After receiving apomorphine, a drug that acts on dopamine receptors, infected mice turned in a pattern linked to one-sided dopamine loss. On a specialized treadmill, they also showed changes in gait, including altered use of a forelimb controlled by the damaged side of the brain.

The virus died out after four weeks, but the movement deficits persisted. That suggests the early infection left lasting physical damage in the brain.

There Is Another

The Texas A&M work adds to a growing effort to understand whether infections can help trigger Parkinson’s in some people, especially when combined with genetics or immune responses.

A separate 2025 Northwestern Medicine study, published in JCI Insight, found Human Pegivirus, or HPgV, in post-mortem brain tissue from five of 10 people with Parkinson’s and none of 14 control subjects with no Parkinson’s. HPgV spreads through blood and belongs to the same viral family as hepatitis C, but researchers have not linked it to any known disease so far.

“HPgV is a common, symptomless infection previously not known to frequently infect the brain,” said Igor Koralnik of Northwestern Medicine. “We were surprised to find it in the brains of Parkinson’s patients at such high frequency and not in the controls.”

The 2025 study also found immune differences in people who carried the virus, including patterns that varied with LRRK2, a Parkinson’s-linked gene.

Together, the two studies ask a provocative but serious question: Can a virus act as an environmental spark for Parkinson’s in a brain already made vulnerable by age, genes or inflammation?

“Viruses are known to cause entirely different diseases based on a person’s genetics,” Brinkmeyer-Langford added.

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What Comes Next

The new TMEV model does not mean a mouse virus causes Parkinson’s in humans. The authors note that TMEV is a natural mouse pathogen with no known effect on people. The study was also small and designed as an early test.

Still, the model gives researchers a way to study a process that toxin models cannot easily show: how infection, immune activity, and dopamine-cell death unfold over time.

Next, the Texas A&M team plans to compare the TMEV model directly with standard Parkinson’s models, search for early warning signs and biomarkers, and study how the immune response to a virus changes 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,” Brinkmeyer-Langford explained.

The bigger implication is that Parkinson’s may not have a single starting point. For some patients, the path may begin with genes. For others, with chemicals. And for some, perhaps, with a viral infection that leaves a lasting mark.

The study was published in the journal Brain, Behavior, & Immunity – Health.