Could a Virus Trigger Parkinson's Disease?

Can a viral infection leave permanent consequences in the brain, even after the body completely eliminates the virus? A new study shows that it can, at least in mice, and reveals how a localized infection was able to destroy neurons important for movement, producing changes very similar to those observed in Parkinson's disease. The discovery offers a new way to study how environmental factors can contribute to the onset of this disease.

Parkinson's disease is one of the best-known neurological diseases and affects more than ten million people worldwide. It occurs mainly because a small group of brain cells, responsible for producing dopamine, begins to die slowly.

Dopamine is a substance essential for controlling body movements. When these neurons disappear, symptoms such as tremors, slowness of gait, muscle rigidity, and balance difficulties arise.

Despite decades of research, scientists still don't know exactly why these cells die. It is known that genetic factors increase the risk in some people, but it is believed that environmental elements also participate in this process. Among them, viral infections have been attracting increasing interest, as several viruses have been linked to alterations in the nervous system and an increased risk of neurological diseases years after infection.

To investigate this hypothesis, the researchers developed an experimental model quite different from the traditional ones. Normally, studies on Parkinson's disease use toxic chemicals that deliberately destroy dopamine-producing neurons, allowing for the rapid reproduction of the disease's symptoms. While these models are extremely useful, they don't represent situations that normally occur in real life.

In this work, the team chose to use a virus naturally found in mice, called Theiler's murine encephalomyelitis virus. This virus was already known to cause inflammation in the nervous system and had been used for many years in research on other neurological diseases, such as multiple sclerosis and epilepsy. The idea was to verify if a viral infection could, by itself, initiate a process similar to that observed in Parkinson's disease.

The experiment was carefully planned. The researchers performed a small surgery on anesthetized mice to introduce a very small amount of the virus directly into only one side of a deep region of the brain called the substantia nigra.

This structure functions as a veritable factory of dopamine-producing neurons. The decision to infect only one side allowed for comparison of the affected part with the healthy part of the same brain, facilitating the identification of changes caused exclusively by the infection. After the virus was applied, the animals were monitored for weeks.

Throughout this period, scientists observed their movements, assessed their motor coordination, and subsequently examined the brain using techniques capable of identifying which neurons remained alive and which had been destroyed.

The results showed that the virus caused exactly the type of damage the researchers were looking to investigate. There was a significant loss of neurons responsible for dopamine production precisely in the region where the virus was applied. As a consequence, the animals began to exhibit difficulties performing normal movements, similar to the alterations observed in classic models of Parkinson's disease.

One of the most interesting aspects was that these motor problems continued even after the organism completely eliminated the virus. This suggests that the infectious agent may act as an initial trigger: it disappears, but the damage caused during the infection remains and continues to affect brain function.

The research also reinforces an idea that has been gaining strength in recent years: perhaps Parkinson's disease does not have a single cause. Instead, it may arise from a combination of genetic predisposition, aging, and environmental factors, such as infections, exposure to toxic substances, or other inflammatory processes.

The authors note that several viruses have already been linked to neurological complications in humans, including influenza, herpes, hepatitis, dengue, and others. This does not mean that these infections directly cause Parkinson's disease, but it indicates that some of them may contribute to creating an environment of prolonged inflammation capable of favoring the degeneration of the most vulnerable neurons.

Finally, the researchers believe that this new experimental model may help answer questions that remain unanswered. Because the disease develops slowly over many years, tracking all stages of this process in humans is extremely difficult.

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Theiler’s murine encephalomyelitis virus as the infectious agent for a virally induced mouse model of Parkinson’s disease

Tae Wook Kang, Rahul Srinivasan, Candice Brinkmeyer-Langford, and C. Jane Welsh

Brain, Behavior & Immunity-Health. Volume 54, July 2026, 101230

DOI:10.1016/j.bbih.2026.101230

Abstract: 

Parkinson's disease (PD) is the second most common neurodegenerative disorder with a prevalence of over ten million patients worldwide. The etiology of PD remains unclear but neuroinflammation specifically associated with viral infection has risen as a possible contributor to the disease. Classical animal models of PD reproduce certain pathophysiological outcomes such as the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc), but these models are limited by the need to inject harmful neurotoxins to induce disease-like symptoms. We present a virally induced neuroinflammatory model of PD in C57BL/6J mice using a naturally occurring pathogen, Theiler's murine encephalomyelitis virus (TMEV), as the infectious agent. This model offers a tool for advancing our understanding of PD pathogenesis and potential treatment options.