Why the Corgi is especially important with regard to degenerative myelopathy (DM)

Corgis represent one of the most important breed groups in degenerative myelopathy (DM) research, especially in the case of the Pembroke Welsh Corgi.

Degenerative myelopathy was originally known mainly in German Shepherd dogs, but from the late 2000s it became clear that the Pembroke Welsh Corgi is one of the most affected breeds. Because of this, many genetic and clinical studies were carried out specifically on Corgis.

According to the scientific literature:

  • the frequency of the SOD1 mutation in the Pembroke Welsh Corgi is among the highest of all the breeds studied;
  • the number of clinical cases is also outstandingly high in this breed;
  • many researchers have studied the natural course of the disease in Corgis.

The Cardigan Welsh Corgi can also carry the SOD1 mutation, but according to most scientific publications:

  • the Pembroke Welsh Corgi has been studied much more thoroughly,
  • more cases have been described in Pembrokes,
  • for the Cardigan, less clinical data is available.

The importance of genetic testing

For the Pembroke Welsh Corgi and the Cardigan Welsh Corgi there is genetic screening for degenerative myelopathy, and today this should be one of the fundamental tests of responsible breeding.

The test primarily examines the following mutation: SOD1:c.118G>A

What exactly does the test examine?

  • whether the dog carries the SOD1 mutation associated with the disease,
  • and if so, in what form.

The results obtainable with the test:

ResultMeaning
N/N (clear)no mutation
A/N (carrier)carrier
A/A (at risk)2 mutant genes

⚠️ An important scientific clarification

“A/A” does NOT definitely mean that the dog will become ill. And a carrier “A/N” does NOT definitely mean that the dog will not become ill!!!!

According to the current consensus:

  • the A/A genotype strongly increases the risk,
  • but the penetrance is not 100%,
  • especially in Corgis the clinical occurrence is indeed higher, but even there the development of the disease is not guaranteed. (vet.cornell.edu)

Where the test is available

1. UC Davis Veterinary Genetics Laboratory (VGL), USA
One of the best-known reference laboratories.

2. Laboratories available in Europe
Several European laboratories also carry out DM screening:

3. Wisdom Panel is a genetic test that can be ordered online, with which you can screen for the diseases of 270 breeds, with particular emphasis on genetic diseases. It can be ordered by post and uses a saliva sample (https://www.wisdompanel.com/en-gb/dog-dna-tests/premium)

Is there a “Corgi-specific” gene mutation?

Currently:

  • in Corgis the same basic SOD1 mutation is the main risk factor,
  • according to several studies there are modifier genes common in the Corgi,
  • which may increase the penetrance,
  • but these are not yet part of standard genetic panels. (pmc.ncbi.nlm.nih.gov)

🧩 What does “modifier gene” mean?

Modifier genes:

  • are genes
  • that do not cause the disease on their own,
  • but can strengthen or weaken the effect of the mutation.

In the Pembroke Welsh Corgi, according to several researchers:

  • there may be population-specific genetic modifiers
  • that increase the penetrance,
  • so that more A/A genotype dogs will actually become ill. (vet.cornell.edu)

The modifier gene in the Corgi

In 2016 an international research group discovered that in Pembroke Welsh Corgis another gene, SP110, significantly modifies the risk of the disease developing.

This means that even between two Corgis with the same SOD1 A/A genotype there can be a significant difference:

  • one of them never becomes ill,
  • in the other the disease may develop at 8–10 years of age.

The difference is partly explained by the SP110 gene variant.

What do geneticists say today?

According to the position of the OFA and the University of Missouri:

  • the A/A result means “high risk”,
  • but it is not a diagnosis,
  • and it does not mean that the dog will certainly develop DM.

This is why the separate DM Risk Modifier (SP110) test was also introduced for Pembroke Welsh Corgis.

What do we see in practice?

In Corgi communities the following regularly occur:

  • A/A dogs that are completely symptom-free up to 13–15 years of age,
  • as well as A/A dogs showing clinical DM at 9–11 years of age.

This is consistent with the scientific observations that the SOD1 mutation is necessary but, on its own, not always sufficient for the disease to develop.

The current scientific consensus

Based on the data available in 2026, experts tend to put it this way:

“The A/A genotype Pembroke Welsh Corgi is predisposed to DM, but the actual outcome is influenced by further genetic factors – especially SP110 – and probably by environmental effects as well.”

In Corgis, SP110 is currently one of the most interesting and most debated “modifier genes” in connection with degenerative myelopathy. This is currently the subject of an active research field.

  • SP110 is NOT the primary cause of DM,
  • but it can probably influence which of the SOD1-mutation dogs will actually become ill,

What is the SP110 gene?

SP110 is a gene involved in:

  • immune regulation,
  • inflammatory responses,
  • nuclear protein regulation.

How did it become associated with DM?

During genetic studies carried out in Corgis it was found that:

  • with the same SOD1 genotype
  • not every dog becomes ill.

This suggested that: other genes may modify the risk.

One of the strongest candidates is SP110.

What does this mean biologically?

SP110:

  • probably influences the immune response,
  • microglial activity,
  • neuroinflammation.

This may modify:

  • how quickly the nerve cells die,
  • when the symptoms appear,
  • how aggressive the DM will be.

Why is it especially important in Corgis?

  • the penetrance is higher,
  • many A/A dogs really do become ill,
  • so the effect of modifier genes can be detected more easily.

According to the researchers: because of the genetic homogeneity of Corgis, the effect of SP110 may be “more visible” than in many other breeds.

Is there a clinical SP110 test?

Currently:

  • there is NO widely validated clinical DM-SP110 test,
  • and SP110 is not part of the standard DM genetic screening.

!!!!!!!! however, Laboklin already performs such a test under the name DMRM (https://laboklin.com/en/products/genetics/hereditary-diseases/dog/degenerative-myelopathy-risk-modifier-dmrm/)

Routine laboratories still examine almost exclusively the SOD1 mutation.

The limits of the DM genetic test:

What can it do?What can it not do?
indicates DM riskpredict disease with certainty
identifies carrierspredict progression
helps breeding decisionsdetermine clinical severity
shows SOD1 statusanalyse modifier genes

The current situation:

GeneEvidence
SOD1strong, proven
SP110promising modifier

What do the breeding guidelines recommend?

The modern genetic recommendation is NOT to exclude every carrier.

But rather:

PairingRecommendation
Clear × Clearideal
Clear × Carrieracceptable
Carrier × Carrierto be avoided
At Risk × anythingstrongly not recommended

Why the Corgi is so severely affected

This is the key question — and here modern genetics comes in.

According to current research, the problem of Corgis is probably NOT that:

  • “they have a different DM mutation”,

but rather that:

  • it is the same SOD1 mutation,
  • but it appears against a different genetic background.

This is why the strange situation occurs that:

DogGenotypeOutcome
Corgi AA/Asevere DM
Corgi BA/Amild or no symptoms

This is one of the strongest pieces of evidence that: DM is not a purely monogenic disease. (pmc.ncbi.nlm.nih.gov)

An interesting scientific problem in Pembroke Welsh Corgis

The Pembroke Welsh Corgi is one of the breeds where the DM mutation is extremely common. In the analysis of a large American database, of the Corgis examined:

  • approximately 6.9% were genetically clear (N/N),
  • 28% were carriers (N/A),
  • 65.1% had the A/A genotype, i.e. were at risk !!!!!!!!

This is one of the reasons why geneticists do not support the immediate exclusion of all A/A dogs: it would remove a significant part of the breed's gene pool from breeding.

What does the OFA say today?

The OFA specifically emphasises that the SP110 test:

  • is relevant only in Pembroke Welsh Corgis,
  • and can only be interpreted in dogs that already have the SOD1 A/A genotype.

In other words:

  • if a Corgi is not A/A, the SP110 result essentially does not change the DM risk;
  • if it is A/A, then SP110 can help to estimate the risk more finely.

Currently it is not known exactly which environmental factors influence the development of DM. Researchers assume that such factors exist because many A/A genotype dogs never become ill, while other, genetically similar dogs do.

“Environmental effect” in this context does not necessarily mean pollution or poisoning, but every non-genetic factor that may affect the ageing of the nervous system or the appearance of the disease.

What has been studied so far?

1. Body weight and obesity

It is assumed that being overweight:

  • may increase the load on the musculoskeletal system,
  • may worsen mobility,
  • may make the neurological symptoms visible more quickly.

At the same time, there is no evidence that obesity in itself would cause DM.

2. Physical activity

Researchers have examined whether:

  • regular exercise,
  • a sporting-dog lifestyle,
  • or, conversely, a sedentary lifestyle

influences the development of the disease.

So far there is no convincing evidence that any of these clearly increases or decreases the risk of DM.

3. Oxidative stress

The SOD1 gene involved in DM plays a role in the cells' defence against oxidative damage. This reaction shows one of the fundamental biochemical roles of the SOD1 enzyme. Because of this, it has been suggested that:

  • cell damage,
  • chronic inflammation,
  • oxidative stress may contribute to the appearance of the disease.

However, this has not yet been clearly demonstrated in dogs.

4. Nutrition

Many owners are interested in:

  • antioxidants,
  • omega-3 fatty acids,
  • vitamin E,
  • special diets.

Currently there is no diet or dietary supplement that has been proven to prevent DM or to stop its development.

Some veterinary neurologists may recommend antioxidants to support general health, but this is not proven DM prevention.

5. Injuries

It is a common misconception that a spinal injury or an accident causes DM.

According to the scientific position:

  • an injury does not cause the disease,
  • but it can make the symptoms of an existing, early-stage DM noticeable sooner.

6. Age

This is the only “environmental” or non-genetic factor whose role is certain.

DM is typically a disease of old age:

  • most affected Corgis are older than 8 years,
  • the peak occurrence is around 10–12 years of age.

This suggests that the ageing of the nervous system is an important part of the process.

What do researchers think today?

According to the current model, the development of DM requires the combined presence of several factors:

  • SOD1 genetic predisposition.
  • Other modifier genes (for example SP110).
  • Biological changes associated with ageing.
  • Probably further, not yet identified environmental factors.

This is similar to how many human neurodegenerative diseases also do not develop because of a single cause.

What can a Corgi owner do?

Based on the current scientific evidence, the most reasonable goals are:

  • maintaining an ideal body weight,
  • regular but not overtaxing exercise,
  • preserving the good condition of the joints and muscles,
  • neurological examinations in old age,
  • monitoring the coordination of the hind legs.

These cannot prevent DM, but they can help preserve the dog's general health and mobility. What is particularly interesting in Pembroke Welsh Corgis: based on the latest research, many neurologists now believe that the genetic background (SOD1 + modifier genes) probably plays a much greater role than the classic environmental factors, so that even between two Corgis living under identical conditions there can be a significant difference in the development of the disease.

What is happening in research now?

In Corgis the following are currently being intensively researched:

  • GWAS (genome-wide association studies),
  • modifier genes,
  • epigenetic factors,
  • neuroinflammation markers,
  • microRNAs,
  • protein aggregation mechanisms.

The goal: to create a future test that:

  • estimates not only SOD1,
  • but also the real clinical risk.

The most important current scientific position

In Corgis:

  • the standard DM genetic test looks at the same SOD1 mutation as in other breeds,
  • but because of the breed's genetic background the clinical effect of the mutation can be stronger.

This is why Corgis are one of the best natural models of ALS-like neurodegeneration.

The most modern research direction

Between 2024 and 2026, increasingly:

  • polygenic risk models,
  • genome-wide association studies (GWAS),
  • modifier gene analyses are being used in Corgis.

The goal: to predict not only the SOD1 mutation, but the actual clinical risk. (nature.com)

References

Important sources

  • Zeng et al. — Breed distribution & modifier research PMC Full Text
  • Coates & Wininger — Canine Degenerative Myelopathy PubMed Abstract
  • Cornell Veterinary Medicine — DM overview Cornell DM Resource
  • UC Davis Veterinary Genetics Laboratory UC Davis DM Genetics