Canine degenerative myelopathy

Degenerative myelopathy (MD or DM) is one of the neurodegenerative conditions
of dogs 8 years and over on average. The progressive degeneration of
neurons in the thoracolumbar region is responsible for ataxia and paresis,
associated with various nervous symptoms such as a decrease in reflexes and
muscle tone, all slowly progressing to flaccid train paralysis
posterior.

Degenerative myelopathy was first described as a disease of the
spinal cord affecting in particular German Shepherds. A predisposition
racial was first identified in the Pembroke Welsh Corgi, the Rhodesian Ridgeback,
the German Shepherd, the Boxer and the Chesepeake Bay Retriever. The clinical entity
“MD” is found in many other breeds; to be able to qualify the disease
of genetics involves proving the association of a mutation in a gene with the disease
described in a given breed. Such research associating histopathology
and genetics are notably carried out by a team from the University of Missouri /
Orthopedic foundation for Animals which was able to show the relationship between a mutation on
the SOD-1 gene and a high risk of developing the disease in dog breeds
following:
American Eskimo Dog, Bernese Mountain Dog, Cardigan Welsh Corgi, Golden Retriever,
Pyrenean Mountain, Kerry Blue Terrier, Poodle, Pug, Shetland Sheepdog
(Sheltie), Soft Coaten Wheaten Terrier, Wire-haired Foxterrier.

For other breeds such as the Saarloos, the Czechoslovakian wolfdog, the Borzoi,
the Hovawart, the Collies and various Bouvier and Shepherd dogs, the mutation into
issue has also been identified; however, it is necessary to cross more
genetic and clinical data to clarify the correlation between the mutation and
disease expression.

In the current state of knowledge, this mutation is associated with a high risk
to develop DM, with incomplete penetrance. Homozygous dogs
normal (N / N) do not have DM, the sick subjects are all of the DM / DM genotype
but conversely, all mutated homozygotes (DM / DM) do not present for
so many troubles.

Two essential criteria are in play: age and genetic background. While most
of dogs show the first symptoms from the age of 8, some older
age 15 are clinically healthy although they carry the mutation. Penetrance and
expressiveness of the disease are regulated by many factors including the genetic background
and living conditions. In other words, foresee the circumstances of appearance
disease in these dogs is impossible and research is focused on identifying
other risk factors within each affected breed.

Since February 2009, LABOKLIN has tested 780 dogs for the SOD-1 mutation with the
following results: 51.5% normal homozygotes, 34% heterozygotes (N / MD)
and 14.5% mutated homozygotes, this distribution varying from race to race.