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Genetic discovery in canine compulsive behavior could yield new insight into human OCD

By Jim Fessenden

UMass Medical School Communications

March 02, 2016

Edward Ginns, MD, PhD

Researchers at UMass Medical School and the Cummings School of Veterinary Medicine at Tufts have identified genetic pathways that exacerbate severity of canine compulsive disorder (CCD) in Doberman pinschers, a discovery that could lead to better therapies for obsessive compulsive disorder (OCD) in people. The findings were published in the International Journal of Applied Research in Veterinary Medicine.

“Genomic research on human neuropsychiatric disorders can be challenging due to the genetic heterogeneity of disease in humans,” said Edward Ginns, MD, PhD, professor of psychiatry and a co-author on the new study. “Canine compulsive disorder shares behavioral hallmarks, pharmacological responsiveness and brain structural homology with human OCD, and thus is expected to be an important animal model.”

OCD is one of the world’s most common neuropsychiatric disorders, affecting an estimated 1 to 3 percent of people and listed by the World Health Organization as among the 20 most disabling diseases. OCD is often characterized by distressing thoughts and time-consuming, repetitive behaviors. Meanwhile, the canine equivalent may include repetitive tail chasing, excessive grooming and flank and blanket sucking.

“Dogs naturally suffer complex diseases, including mental disorders that are similar to those in humans. Among those is canine compulsive disorder, the counterpart to human obsessive compulsive disorder,” said the study’s first and corresponding author Nicholas Dodman, BVMS, DACVA, DACVB, professor in clinical sciences and section head and program director of animal behavior at Cummings School.

The research team compared whole genome sequencing of 70 Doberman pinschers to search for inherited factors that exacerbate CCD. Researchers identified two genetic loci strongly correlated with severe CCD, as well as a third locus that showed evidence of association.

The locus most strongly associated with severe CCD was found on chromosome 34, a region containing three serotonin receptor genes.

“This is particularly significant because drugs that work on the serotonin system are the mainstay treatment for OCD in humans, which demonstrates further correlation between the human and animal models,” said Dr. Dodman.

The second locus significantly correlated with severe CCD was on chromosome 11, the same chromosome that contains a gene thought to increase the risk of schizophrenia in humans. This discovery, along with suggestive evidence found on chromosome 16 linking CCD to stress tolerance, may also be relevant to the pathophysiology of OCD, according to the study authors.  

“Comparative genomics is a particularly attractive approach to reveal the molecular underpinnings of disease in inbred animals with the hope of gaining new insights into these diseases in dogs and humans that lead to better treatments,” said Dr. Ginns.

The study builds on more than a decade of research from Cummings School and UMMS. In 2010, Dodman and Ginns identified that the neural cadherin (CDH2) gene on chromosome 7 appeared essential for susceptibility to the condition.

“If the canine construct is fully accepted by other OCD researchers, this spontaneously-occurring model of the condition in humans, right down to the biological pathways involved, could help point the way to novel and more effective treatments for such a debilitating condition,” Dodman said.