Texas A&M vet research team study suggests link between viral infection and ALS
Veterinary researchers at Texas A&M University are at the center of a major scientific discovery that could reshape how we understand and eventually treat devastating motor neuron diseases like amyotrophic lateral sclerosis (ALS).
A large, multidisciplinary team led by scientists across Texas A&M, including several veterinary researchers from the College of Veterinary Medicine & Biomedical Sciences, has identified a unique mouse model that closely mirrors how ALS develops in humans. The finding highlights the powerful role veterinarians play in advancing both animal and human health.
A Mouse Model That Mimics Human ALS
The team discovered that a specific mouse strain, known as CC023, responds to a viral infection in a way that looks strikingly similar to ALS in people. After infection, these mice developed lasting neurological damage and muscle wasting — even after the virus itself was cleared.
“This is exciting because this is the first animal model that supports the long-standing theory that a viral infection can trigger permanent neurological disease long after the infection has resolved,” said Candice Brinkmeyer-Langford, a neurodegenerative disease expert at Texas A&M.
For veterinarians and physician-scientists alike, this model offers a rare and valuable opportunity: a living system that allows researchers to study how genetics, immune response, and infection interact to cause chronic neurodegenerative disease.
Why This Matters
More than 90% of ALS cases are sporadic, meaning they are not inherited. Until now, scientists have struggled to model how environmental triggers like viruses might contribute to the disease.
The CC023 mouse strain provides a new “test track” for:
Identifying early biomarkers of ALS
Studying how immune responses cause long-term nerve damage
Testing potential therapies before irreversible damage occurs
Veterinary Science at the Core of the Study
To conduct the research, the team — including multiple veterinary pathologists, immunologists, and biomedical scientists — infected five genetically diverse mouse strains with Theiler’s murine encephalomyelitis virus (TMEV). They then tracked disease progression across acute, subacute, and chronic stages.
Using advanced veterinary pathology and comparative medicine techniques, the researchers evaluated:
Spinal cord inflammation
Viral load
Severity of paralysis and muscle loss
Differences in immune response between strains
Key Findings from the Study
The veterinary-led research revealed four major insights:
Early nerve damage: All strains showed spinal cord injury within two weeks of infection.
Permanent muscle loss: CC023 mice developed lasting muscle wasting, even after the virus was cleared.
ALS-like pathology: Lesions and clinical signs closely resembled those seen in human ALS patients.
Immune shutdown: Immune cells were highly active early on, but damaging effects persisted after viral clearance.
In short: the virus lit the match, but genetics determined the fire.
Genetics Matter and Veterinarians Are Leading the Way
“This study gives us a new way to understand how viral infections can cause lasting damage to the spinal cord, nerves, and muscles in genetically susceptible individuals,” Brinkmeyer-Langford said.
The work underscores the critical role veterinarians play in comparative and translational medicine, bridging animal models and human disease to unlock answers that medicine alone can’t reach.
A Truly Collaborative Effort
The study, published in the Journal of Neuropathology & Experimental Neurology, was led by veterinary researchers Koedi S. Lawley and Tae Wook Kang, alongside a team of experts from Texas A&M’s College of Veterinary Medicine & Biomedical Sciences and collaborating institutions.
Funding was provided by the National Institute of Neurological Disorders and Stroke, the National Institute of Environmental Health Sciences, and the National Science Foundation.
