Leonberger Polyneuropathy    from the CHF website

University of Minnesota (University)

Active Grant No: 920:

Genetic Basis of Polyneuropathy in Leonbergers

Disease(s):  Neurological Disease

Sponsor(s):

Leonberger Health Foundation

Researcher(s):  James R. Mickelson, PhD

Breed(s): Leonberger

Abstract:

 We propose to use the most current gene identification strategy enabled by the canine genome sequencing and mapping project to find the locations of genes causing susceptibility of polyneuropathy in Leonbergers (LPN). The ultimate goal is to develop DNA-based tests for susceptibility to LPN that can be used in breeding decisions to help reduce its incidence and potentially for more specific therapies to address the condition.

July 1st 2008 Update Report for Sponsor:

Grant 0920:

We are using the most current gene identification strategy enabled by the canine genome project, termed SNP chips, to find the chromosomal locations of gene(s) causing susceptibility to polyneuropathy in Leonberger dogs (LPN).  The ultimate goal is to develop DNA-based tests for susceptibility to LPN that can be used in breeding decisions to help reduce its incidence and potentially for more specific therapies to address the condition.

The good news is that with the outstanding help of the breed club we are making excellent progress on acquiring sufficient samples for the SNP chip gene mapping experiments.  Encouraging owners to have both symptomatic “presumed affected” as well as asymptomatic “presumed normal” dogs biopsied to confirm this status would be a tremendous help to us in these studies.  The less good news is that although we have started using the SNP chips we have not yet found LPN gene locations on the chromosomes with sufficient confidence.  Although several possible chromosomes have been indicated, none stands out more than any other with the limited data to date.

A major factor impacting the project is that the genetic model for inheritance of LPN (i.e., whether it is autosomal recessive or sex-linked, or polygenic, etc) is not currently known.  An optimistic scenario at the beginning of our studies was that LPN would be a relatively simple trait with only one or two major genes contributing to the condition, and if so, the gene loci might be able to be mapped with relatively few samples.  We still do not know the best genetic model to explain LPN, but feel it possible that LPN might not be as simple as hoped.  So, we will continue with genotyping additional samples on the SNP chips to attempt to map the disease gene loci, and we hope to have these results in the near future.

Leonberger Research Biopsy Sub Form


Polyneuropathy Report March 2008