University of Missouri researchers believe that a genetic mutation found in Tibetan Terriers is the same gene responsible for the development of Parkinson’s disease in humans. Researchers within the Department of Veterinary Medicine recently published their results in Neurobiology of Disease, arguing that this discovery could lead to treatment benefits for both canine and human sufferers in the near future, ScienceDaily reports.
The canine disease, commonly seen in Tibetan Terriers, is called adult-onset neuronal ceriod-lipofuscinosis (NCL). The degenerative neurological disease develops in dogs around age 5, leading to symptoms of dementia, impaired vision, unwarranted aggression, loss of coordination and seizures. Initial signs of the disease are often observed as increased shyness and sudden loss of muscle control. The disease progresses due to nerve cell failure to “recycle” material that builds up in the brain and eyes, creating plaques that interfere with cell function.
Lynn Steinhaus’s dog Topper suffered from the disease that claimed his life in 2009. “This is a really hard disease for dog owners to go through,” she said. “Those seizures are just terrible.” Steinhaus said she first noticed that Topper was becoming increasingly more shy around age five, and later showed losses in muscle control and coordination. Topper eventually began to have seizures of increasing frequency and was euthanized about a year later. His DNA was used for the purposes of this study.
The symptoms of NCL in humans and dogs are similar, ultimately leading to death in both species. There are many types of NCL in humans, but dogs only suffer from one type and researchers were able to use DNA samples from known canine sufferers to pinpoint the specific genetic mutation linked to the disease. The mutation discovered in dogs with NCL causes the hereditary form of Parkinson’s disease in humans, suggesting that the plaque formation seen in dogs with NCL might be the same problem in humans with Parkinson’s.
Researchers believe that potential human therapies could be tested on the canine population, as DNA testing for dogs can identify dogs that will be affected by NCL before they start to show symptoms. Co-author O’Brian said “Dogs and people suffer form the same diseases, and it’s much easier to discover gene issues in dogs because of the unique genetics of pure-bred dogs. Because we have a medical and veterinary school near each other, we can find the genes in the dog and then find out if they cause a similar disease in people.”
Martin Katz, professor of pathobiology at the University of Missouri described the results of the collaborative effort, stating that “Finding that gene was like finding a single house in a very large city- but we had the dog family history and the tools to look through the city in a systematic way to locate the address of the mutation responsible for the disease.” The publication is the result of 10 years of research and the collaboration between many human and veterinary scientists at the University of Missouri.
