Describes a Theiler's murine encephalomyelitis virus (TMEV) infection in C57BL/6J mice that produces neuroinflammation and dopaminergic neuron loss in the substantia nigra as a non-toxin model of Parkinson-like pathology.

Offers a translationally relevant, infection-driven platform to study inflammation-mediated PD mechanisms and to test anti-inflammatory/antiviral or neuroprotective interventions, though its value hinges on how well it reproduces key PD features (e.g., alpha-synuclein aggregation, progressive…

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.