DM clear vs carrier - Page 4

ANALYSIS  PARALYSIS 
                           
          If you have enough money and a research team you can find anything and everything. Does that mean it will change things much probably not because people don't use what they have now to make a breed better. What is going to happen when they keep finding labels to match diseases or diseases to put names to. I know as humans we dont want to admit we aren't in control but we have to accept that things are impermanent and evolving. The Dogs will be fine i think it's the human condition that has the disease of not being at ease with a little bit of knowledge.
 

                                                                       Grooving Lovin Life

"Unless I am misunderstanding Joanro, the DM test does not test for GSD DM, so it doesn't sound like it is likely to be any help to GSD breeders. Is there any evidence that GSDs suffer from any other type of DM?"

Yes, they can suffer from either. My point was that these are two separate conditions; why not test for the one we can and for both when/if we ever get that capability?

I don't see how you could make that claim, considering the subjects with false positive results, who test positive as carriers and never develop the DM condition.

Daryl, supposedly, it is a recessive gene, so a "carrier" would not get DM. Supposedly it takes two alleles for the disease to manifest itself.....in breeds other than the GSD, according to studies.

If it is in question of even a remote possibility of the puppies being affected by this horrific disease why not test the pups you are interested in buying in the litter,  it is a small price to pay for piece of mind.  Nan

Puppies can be tested as early as 4 weeks old.  Yeah...

Why test the pups if the parents are tested and you haven't bred anything which will produce "at risk". Studies claim that even "clear" dogs have developed DM. So, I'm thinking that this is not accurate, at best and at worst, gives false sense of security.

I guess I'm confused.  I would have thought a carrier simply a carrier too, but I thought that's what "at risk" was supposed to mean.  "Positive" or whatever is what I meant to say.

So if a dog can test clear and still develop DM, does that mean it can, and probably has, passed it on to it's progeny who may, or may not, test clear.?  If this can happen, presumeably a dog can test as at risk and never develop it, does that mean such a dog will pass it on?  Sorry, I don't think this test sounds reliable enough to make a decision to use or discard a tested dog based on the results.

Margaret N-J

Kaffir, don't "discard a tested dog based on results". This test is not reliable by the proclamations of the very researchers. Just don't breed anything the will produce "at risk" just in case the researchers decide that it does have merit for GSD. JMO.

Can anyone point me to some reading on the gsd-specific DM?? I wasn't aware of this prior to this thread, so I'd def like to investigate!!

Thanks!

Here's a couple excerpts from a recent paper published in Febuary

Genome-wide association studies for multiple diseases of the German Shepherd Dog

Degenerative myelopathy (DM) is a late-onset neurodegenerative disease characterized by ataxia and weakness in the hind limbs. Symptoms of DM worsen over time, either steadily or in phases, and eventually result in complete paraplegia. In some cases, DM may progress up the spinal cord and cause forelimb weakness or even respiratory difficulties (Barclay and Haines 1994). The age of onset of DM is generally between 5 and 14 years, with a mean age of onset of 9 years (Averill 1973). The clinical signs observed in DM are general indicators of spinal cord disorders, but a definitive diagnosis for DM can be made only by histopathological examination of spinal cord tissue postmortem (Coates et al. 2007). Most owners of affected dogs elect euthanasia within several months of symptom onset (Johnston et al. 2000). DM is most prevalent in the GSD (Coates et al. 2007). A recessive missense mutation in SOD1 is associated with DM in several breeds, including the GSD (Awano et al. 2009). DM has been proposed to be an animal model for amyotrophic lateral sclerosis (ALS). Approximately 20% of hereditary ALS cases are attributed to mutation of SOD1 (Rosen et al. 1993).
 

Degenerative myelopathy

GWAS with 100,000 permutations for DM was carried out using all cases collected (n = 15) versus control dogs that were at least 8 years of age and did not exhibit any clinical signs of DM (n = 69). The two strongest associations are with SNPs 31.28909487 (P_raw = 8.51 × 10⁻⁰⁶, P_genome = 0.1461) and 31.30528862 (P_raw = 5.59 × 10⁻⁰⁵, P_genome = 0.5771) (Fig. 3a). These SNPs on Chr 31 are located 650 kb upstream and 965 kb downstream of SOD1, respectively. Evaluation of individual genotypes in this region reveals that only 4 of the 15 cases are homozygous for both SNPs. Five cases are homozygous for the associated allele of SNP 31.30528862, while nine cases are homozygous for the associated allele of SNP 31.28909487. In the control population, 6 of 69 GSDs are also homozygous for the same allele of SNP 31.28909487. A third noteworthy result is on Chr 10 for SNP 10.64801770 (P_raw = 6.06 × 10⁻⁰⁵, P_genome = 0.6066).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509149/