[ SHOWGSD-L ] More on Degenerative Myelopathy

  • From: Ginialtman@xxxxxxx
  • To: TISHW@xxxxxxx, d_fritsche@xxxxxxxxxx, DKARLOFF@xxxxxxx, marhaven@xxxxxxxxxxxxxx, showgsd-l@xxxxxxxxxxxxx
  • Date: Sat, 9 Aug 2008 11:33:39 EDT

I wanted to share with you the way I understand the differences between the  
Corgi, Boxer DM and the GSDM. I also comment briefly on the OFA and Broad  
Institute test. I have heard from Dr Clemmons again-- I asked him to let me 
know  
if I am reflecting this information correctly --and he confirmed that as well 
as  to have clarified some stuff for me -- specifically about the early onset 
 vs the typical disease in the GSD. So this is what I think all the  
technical stuff means. (second read with corrections and clarification for  
some:-)
 
If I am understanding completely the most recent stuff I have from Dr.  
Clemmons, he is speculating that the DM in German Shepherd Dogs involves a  
number 
of genetic markers (many of which he has found) and that there are  changes in 
other genes locations in addition to the changes (likened to ALS or  Lou 
Gehrig's) described for the Corgi and Boxer. Even in the Boxer and Corgi  (and 
certainly in the GSD) the SOD1 gene change does not fully explain the  disease. 
GSDM is like Primary Progressive Multiple Sclerosis in the way that the  
disease manifests itself and the cells that the disease targets are the same as 
 for 
PPMS. I cite Dr. Clemmons because he is a neurologist and his life's work  
has been DM in the German Shepherd Dog. He is trying to explain all of the  
changes which have been found and reported in GSDM, not just to make the 
disease  
fit one genetic finding.
Dr. Clemmons is not saying that there are two types of DM for the GSD.  I 
think he is looking at the other research and other genetic findings in order  
determine the genetic make up of the disease. While 2 forms of DM have been  
described in the GSD, an early juvenile form and the typical disease in older  
dogs, these appear to be separate conditions. The juvenile disease may have  
different genetics. It is the adult onset disease which has been recognized as  
GSDM. It is this disease which is like PPMS and is related to an immune attack  
upon the spinal cord. Clemmonsâ?? speculates that the SOD1 gene (which is a 
likely  target for his genetic test) acts as the immune trigger which 
sensitizes 
the  body against its own nervous system and leads to GSDM. Other changes are 
needed  for the disease to manifest, since most of the dogs with the SOD1 
change do not  get the disease. This may be due to a process called â??gene 
imprintingâ?? where  some other genes turn on or off and it is the combination 
of all 
the gene  changes that lead to clinical GSDM. So, the research into the 
genetics 
of GSDM  is far from complete if we are to eventually find out which GSDs are 
most likely  to contract GSDM. 

I also read with interest that Dr. Clemmons applauds that work is being  done 
by others. And now that we have given him funding, his research will  
contribute to the full knowledge of the disease in GSD. As for the OFA 
testâ??the  way 
I read it--they are inviting participation by specific breeds-- not that  they 
are "recommending" it necessarily but that it is pertinent for the breeds  
mentioned. 
 
I think it is too early to speculate that for GSD we have a tool by either  
Broad Institute or the U of Florida that will allow us to determine the cause 
of  the disease or even a certain mode of inheritance or factors for prediction 
of  disease. Genetic testing for the purpose of elimination of carriers is 
not yet  appropriate. That may be the outcome of all of this work and it 
certainly is  beneficial that all of this interest has surfaced in the disease 
of DM. 
What we  do know is that two different researchers have found changes in 
genes in the GSD  that needs additional study. If you have a dog that  
qualifies--participate!!
 
Ginny Altman

"Please let me be as kind,  intelligent, and wonderful as my dog thinks I  
am."



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