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.
