Degenerative Myelopathy (DM) and the SOD1 DNA Test in Finnish Lapphunds

Understanding the science behind one of the breed's most misunderstood DNA tests

Degenerative Myelopathy (DM) is one of the most misunderstood health topics within the Finnish Lapphund breed.

As commercial DNA testing has become increasingly common, many puppy owners now receive genetic reports from companies such as Embark, Orivet and other laboratories that include a result for Degenerative Myelopathy (SOD1). It is also becoming increasingly common for prospective owners to ask breeders about DM after reading online articles, social media discussions or using AI tools such as ChatGPT.

This has led to understandable confusion.

If a DNA report includes a result for Degenerative Myelopathy, surely it must be an important disease for the breed?

Why do responsible Finnish Lapphund breeders place considerable emphasis on DNA tests such as prcd-Progressive Retinal Atrophy (prcd-PRA), yet often place relatively little emphasis on the SOD1 result?

Is the DNA test unreliable?

Should breeders only use "DM Clear" dogs?

Or is the answer more complicated?

The reality is that the science surrounding Degenerative Myelopathy is considerably more nuanced than many people realise.

The SOD1 DNA test does not test for Degenerative Myelopathy itself. Instead, it identifies a mutation that has been associated with an increased risk of developing the disease in some breeds. Whether that association exists, and to what extent, depends on the breed of the dog.

This distinction is the foundation of the entire discussion. Understanding this distinction explains why breeders place considerable emphasis on some DNA tests while interpreting others very differently.

For Finnish Lapphunds, the relationship between the SOD1 mutation and Degenerative Myelopathy has not been scientifically validated. At the same time, confirmed cases of the disease remain exceptionally rare worldwide despite many dogs carrying the mutation.

Understanding why requires a basic understanding of genetics, how DNA tests are developed and validated, and how responsible breeding decisions are made.

This article brings together the currently available scientific evidence, published literature and breed specific information relating to Degenerative Myelopathy in Finnish Lapphunds.

Its aim is to explain what the SOD1 DNA test measures, why it differs from validated DNA tests such as prcd-Progressive Retinal Atrophy (prcd-PRA) and Pompe Disease, and what the available evidence tells us about its significance within the breed.

Key Takeaways

If you only read one section of this article, read this.

✔ The SOD1 DNA test does not test for Degenerative Myelopathy itself.

✔ It identifies a mutation that has been associated with increased disease risk in some breeds.

✔ That association has not been validated for Finnish Lapphunds.

✔ The SOD1 mutation occurs more commonly than Degenerative Myelopathy itself within the breed.

✔ Breeders therefore place greater emphasis on health tests that have been validated for Finnish Lapphunds, while continuing to monitor emerging research.

✔ A DNA test can be scientifically accurate, yet not clinically useful for every breed.

Understanding DNA Testing

Before discussing Degenerative Myelopathy specifically, it is helpful to understand what a DNA test actually measures. Commercial DNA tests do not diagnose disease. Instead, they examine a dog's DNA and look for specific genetic variants (sometimes referred to as mutations) that researchers have identified and chosen to include in the testing panel.

Every dog carries approximately 20,000 genes. These genes contain the instructions that tell the body how to grow, develop and function throughout life. Just as no two people are genetically identical, every dog also carries thousands of naturally occurring genetic differences.

Most of these genetic differences have no effect on health whatsoever. Some influence simple characteristics such as coat colour or coat length. Others may increase the likelihood of developing a particular disease, while a small number are directly responsible for causing inherited conditions.

This is where many misunderstandings begin.

Finding a genetic variant does not automatically mean that a dog has a disease, or even that it will ever develop that disease.

Instead, the significance of any DNA result depends entirely on what researchers know about that particular variant.

In some cases, researchers have demonstrated that a specific mutation directly causes disease within a breed. In these situations, DNA testing becomes an extremely reliable tool for responsible breeding.

In other cases, researchers have identified a genetic variant that appears to be associated with an increased risk of disease, but the relationship is not straightforward. Other genes, environmental influences or biological factors may determine whether the disease ever develops.

Finally, some genetic variants are identified simply because they exist. Until sufficient research has been completed, their significance for a particular breed may remain uncertain.

Understanding which of these categories a DNA test falls into is far more important than simply knowing whether a dog is genetically "clear", a "carrier" or "at risk".

Throughout this article, one of the key themes will be that not all DNA tests provide the same level of information.

Some DNA tests have been scientifically validated as reliable predictors of disease within a breed and can therefore be used confidently in breeding decisions.

Others identify genetic variants that are scientifically interesting but whose significance within a particular breed has not yet been established.

Understanding the difference between these two situations is essential to understanding why Finnish Lapphund breeders treat the SOD1 result differently from DNA tests such as prcd-PRA and Pompe Disease.

Why does validation have to be breed-specific?

One of the most common misconceptions surrounding canine DNA testing is that if a laboratory reports a genetic result, the test must automatically be useful for every breed.

In reality, that is not how genetic testing works.

A DNA laboratory can accurately identify a genetic mutation, but that does not necessarily mean the mutation is a reliable predictor of disease in every breed. To understand why, it helps to know what scientists mean when they say a DNA test has been validated. Validation is the process of demonstrating that a particular genetic variant consistently predicts the presence, absence or risk of developing a disease within a specific breed. Finding a mutation is only the beginning.

Researchers must then determine whether that mutation is actually responsible for causing the disease, or whether it is simply associated with it. They do this by studying large numbers of dogs, including both affected and unaffected individuals, and comparing their DNA results.

If the mutation is found consistently in affected dogs, and absent from unaffected dogs, researchers can be confident that the mutation is a reliable predictor of disease within that breed. Only then can the DNA test be considered a reliable tool for making breeding decisions.

This process must be repeated for each breed.

Although all dogs belong to the same species (Canis lupus familiaris), each breed represents a genetically distinct population with its own history, founder animals, inherited diseases and unique patterns of genetic variation. Through generations of selective breeding, each breed has developed its own genetic profile.

This is why many DNA tests are developed and validated on a breed by breed basis.

A mutation that is strongly associated with disease in one breed cannot automatically be assumed to have the same significance in another.

This distinction is fundamental to understanding the difference between tests such as prcd-Progressive Retinal Atrophy (prcd-PRA) and the SOD1 mutation associated with Degenerative Myelopathy.

For prcd-PRA, researchers have demonstrated that the mutation is responsible for causing the disease in Finnish Lapphunds. The inheritance pattern is well understood and predictable. Breeders can therefore use the DNA test with confidence to avoid producing affected puppies while maintaining genetic diversity.

The situation with SOD1 is different.

Although the mutation can be accurately detected by commercial DNA laboratories, there is currently no published evidence demonstrating that the mutation reliably predicts the development of Degenerative Myelopathy in Finnish Lapphunds.

This does not mean the laboratory is incorrect. And it does not mean the mutation does not exist.

It simply means that the relationship between the mutation and the disease has not yet been established for Finnish Lapphunds.

This distinction is often overlooked, but it is one of the most important concepts in canine genetics.

A DNA test can be scientifically accurate while its clinical significance remains undetermined.

In other words, the laboratory can correctly identify a mutation without researchers yet knowing exactly what that mutation means for the health of a particular breed.

The presence of a DNA result on a commercial report should therefore never be confused with evidence that the result is clinically meaningful for every breed.

What Does the SOD1 DNA Test Actually Measure?

One of the biggest misconceptions surrounding Degenerative Myelopathy is that the DNA test detects the disease itself.

It does not. The DNA test identifies whether a dog carries a specific mutation within a gene called SOD1 (Superoxide Dismutase 1).

This is an important distinction because a gene and a disease are not the same thing.

The SOD1 gene is a normal part of every dog's DNA. It contains the instructions for producing the superoxide dismutase enzyme, one of the body's natural antioxidant enzymes. This enzyme helps protect cells by neutralising unstable molecules known as reactive oxygen species, or "free radicals", which are produced during normal metabolism.

In other words, SOD1 performs an important housekeeping role throughout the body and is not a "Degenerative Myelopathy gene".

The DNA test does not measure how well the enzyme functions, nor does it diagnose Degenerative Myelopathy.

Instead, it looks for one particular mutation within the SOD1 gene that researchers have associated with an increased risk of developing Degenerative Myelopathy in some breeds.

This distinction is critical.

The DNA test tells us that a mutation is present.

It does not tell us whether the dog has Degenerative Myelopathy.

It does not tell us whether the dog will develop Degenerative Myelopathy.

It does not tell us whether that mutation has the same significance in every breed.

Those questions require scientific research beyond the DNA test itself.

A mutation does not always equal disease

Another common misunderstanding is that identifying a mutation automatically means researchers have identified the cause of a disease. This is not always the case.

Some mutations are directly responsible for causing inherited diseases. Others are associated with an increased risk but require additional genetic or environmental factors before disease develops. Others may simply occur alongside a disease without being its direct cause.

Current evidence suggests that the SOD1 mutation falls into the second category.

Even in breeds where the association between the SOD1 mutation and Degenerative Myelopathy has been well established, the mutation is not fully predictive. Many dogs carrying two copies of the mutation ("at risk") never develop Degenerative Myelopathy during their lifetime.

Conversely, there have been occasional reports of dogs developing clinical signs consistent with Degenerative Myelopathy despite not having the expected genetic result. This phenomenon is known as incomplete penetrance.

In simple terms, incomplete penetrance means that carrying a mutation does not guarantee that disease will develop.

Researchers believe that additional genes, biological pathways and environmental influences all contribute to determining whether a dog ultimately becomes affected.

For Finnish Lapphunds, the relationship is even less clear.

While the SOD1 mutation can be detected by commercial DNA laboratories, there is currently no published evidence demonstrating that it reliably predicts the development of Degenerative Myelopathy in Finnish Lapphunds.

This is why the presence of an SOD1 result on a DNA report should never be interpreted in isolation. The mutation is one piece of information.

Understanding what that information actually means requires looking at the scientific evidence for the breed in which it occurs.

When the SOD1 Test First Became Available

During the mid to late 2010s, commercial DNA testing expanded rapidly. Laboratories began offering increasingly comprehensive testing panels, screening for hundreds of genetic variants across many different breeds. Around this time, the SOD1 mutation associated with Degenerative Myelopathy was added to the DNA panels offered for Finnish Lapphunds.

For Finnish Lapphund breeders, this was the first time they had encountered a DNA result relating to Degenerative Myelopathy. The natural reaction was curiosity and concern.

Like any responsible breeder, Finnish Lapphund breeders wanted to understand what this new result meant for the breed and whether it should influence breeding decisions. Initially, there was understandable uncertainty.

The SOD1 result appeared alongside well established DNA tests such as prcd-PRA, leading some to assume it should be interpreted in the same way. After all, if a commercial DNA laboratory was reporting the result, it seemed reasonable to think it must carry the same level of importance.

Rather than accepting that assumption, breeders, breed clubs and health coordinators began looking more closely at the available evidence.

Information was sought from veterinary specialists, geneticists, published scientific literature and international breed health committees. Just as importantly, breeders looked at what was actually being observed within the Finnish Lapphund population.

The picture that emerged was very different from diseases such as prcd-PRA.

While the SOD1 mutation was being identified in a proportion of Finnish Lapphunds, confirmed cases of Degenerative Myelopathy remained exceptionally rare. The expected relationship between the DNA result and the disease simply was not being seen within the breed.

This prompted an important question: If the SOD1 mutation were a strong predictor of Degenerative Myelopathy in Finnish Lapphunds, why were so few dogs developing the disease?

That question has continued to guide research and discussion ever since.

As additional information became available, it became increasingly apparent that the SOD1 result should not be interpreted in the same way as validated DNA tests such as prcd-PRA. While the mutation could be accurately detected, there was no published evidence demonstrating that it reliably predicted Degenerative Myelopathy in Finnish Lapphunds.

This understanding has shaped the approach taken by many responsible Finnish Lapphund breeders today. Rather than treating the SOD1 result as a stand alone breeding tool, it is considered alongside the current scientific evidence, the known health of the breed and the importance of preserving long term genetic diversity.

What Does the Evidence Tell Us?

Ultimately, the usefulness of any DNA test comes down to one simple question: Does the result reliably predict disease within the breed?

This is where the evidence for Finnish Lapphunds becomes particularly interesting.

Since the SOD1 mutation was introduced into commercial DNA testing panels, large numbers of Finnish Lapphunds around the world have been tested. These results have shown that the mutation is common within the breed. Dogs carrying one or two copies of the mutation are regularly identified.

If the SOD1 mutation were a strong predictor of Degenerative Myelopathy in Finnish Lapphunds, we would expect to see a corresponding number of affected dogs. That has not been observed. Instead, confirmed cases of Degenerative Myelopathy remain exceptionally rare worldwide.

Historically, only a very small number of confirmed cases have been reported internationally despite many years of DNA testing and widespread use of commercial genetic screening. I am not aware of any confirmed cases being diagnosed in Australia.

This creates an important disconnect.

On one hand, the SOD1 mutation is present in a reasonable proportion of the breed.

On the other, Degenerative Myelopathy itself remains an exceptionally uncommon diagnosis.

If the mutation behaved in Finnish Lapphunds as it does in breeds where the association has been scientifically validated, these two observations would be expected to align much more closely.

Instead, they do not.

Taken together, the available evidence suggests that the SOD1 mutation does not have the same clinical significance in Finnish Lapphunds as it does in breeds such as the German Shepherd Dog or Pembroke Welsh Corgi.

Of course, the absence of evidence is not the same as evidence of absence. It remains entirely possible that the SOD1 mutation contributes to Degenerative Myelopathy in Finnish Lapphunds in some way. However, if it does, the currently available evidence suggests that the relationship is likely to be considerably more complex than a simple cause and effect mutation.

Researchers believe that additional genetic factors, biological pathways and environmental influences are likely to play an important role in determining whether disease develops. This is supported by observations from other breeds, where many dogs carrying two copies of the SOD1 mutation never develop Degenerative Myelopathy despite living to old age.

Taken together, the available evidence suggests that the SOD1 mutation alone is not a reliable predictor of Degenerative Myelopathy in Finnish Lapphunds.

Importantly, this conclusion is based not on a single study or opinion, but on the combination of several observations:

the disease remains exceptionally rare within the breed;
the SOD1 mutation occurs vastly more frequently than the disease itself;
there is currently no published validation demonstrating that the mutation reliably predicts disease in Finnish Lapphunds; and
even in breeds where the association has been validated, the mutation is not fully predictive and additional factors clearly influence whether disease develops.

This explains why breeders place greater emphasis on DNA tests that have been scientifically validated for Finnish Lapphunds while continuing to monitor new research into Degenerative Myelopathy.

Importantly, the burden of proof lies with demonstrating that a DNA test reliably predicts disease within a breed, not with proving that it does not.

Why the rarity of the disease matters

The usefulness of any DNA test depends not only on whether a mutation is associated with disease, but also on how common the disease is within the population being studied.

In breeds where Degenerative Myelopathy occurs relatively frequently, researchers can compare large numbers of affected and unaffected dogs to determine how well a genetic mutation predicts disease. This is one of the reasons the SOD1 mutation has been successfully validated in breeds such as the German Shepherd Dog.

Finnish Lapphunds present a very different situation.

When a disease is exceptionally rare, demonstrating that a mutation reliably predicts disease becomes much more difficult. A mutation may be present, but unless it consistently corresponds with disease, its practical value as a predictive breeding tool remains uncertain.

This is another reason why breed-specific validation is so important. The value of a DNA test depends not simply on whether a mutation exists, but on how accurately that mutation predicts disease within the breed being tested.

Why Responsible Breeding Is About More Than One DNA Test

One of the most common questions people ask is:

"If the SOD1 mutation exists, why don't breeders simply eliminate it from the breed?"

At first glance, this seems like a sensible solution. However, responsible breeding is rarely that simple. Every dog is far more than the result of a single DNA test.

A dog represents thousands of genes, together with its temperament, structure, health, longevity, breed type and genetic contribution to future generations.

Every time a breeder chooses one dog over another, they are selecting all of those characteristics together.

This is one of the fundamental principles of population genetics.

Selecting strongly for one characteristic inevitably means selecting against something else.

The challenge for breeders is deciding which traits should be prioritised while maintaining the long term health of the breed as a whole.

Every breeding decision involves compromise

Imagine a breeder has two otherwise excellent dogs. One carries the SOD1 mutation. The other does not.

If there is no evidence that the SOD1 mutation predicts disease in Finnish Lapphunds, should the first dog automatically be removed from the breeding population?

Geneticists would say no.

That decision would also remove every other valuable characteristic carried by that dog.

Perhaps it has outstanding hip and elbow scores.

Perhaps it has excellent ACES eye examination results.

Perhaps it comes from a long lived family with exceptional temperament.

Perhaps it represents an important bloodline that helps maintain genetic diversity within the breed.

Discarding all of those qualities based solely on a DNA result that has not been validated for the breed could do more harm than good.

Why genetic diversity matters

One of the greatest challenges facing purebred dogs is maintaining healthy levels of genetic diversity.

Every breed begins with a relatively small number of founder animals.

Over many generations, breeders inevitably make selections for health, temperament and breed type.

While selection is an essential part of responsible breeding, excessive selection can gradually reduce genetic diversity.

This is important because genetic diversity is closely linked to the long term health of a population.

A genetically diverse breed is generally better equipped to maintain fertility, immune function and overall resilience while reducing the accumulation of undesirable inherited traits.

Conversely, removing large numbers of otherwise healthy dogs from the breeding population can unintentionally narrow the gene pool.

For this reason, modern canine population genetics encourages breeders to preserve as much healthy genetic diversity as possible while making evidence based health decisions.

Why "clear" does not automatically mean "better"

It is understandable why puppy buyers are drawn to the word "clear."

It sounds reassuring.

However, a genetically clear result for one particular mutation does not automatically make one dog healthier than another.

A dog that is genetically clear for the SOD1 mutation may still carry other inherited conditions, have poorer hip scores, less desirable temperament, or contribute less to the long term genetic diversity of the breed.

Likewise, a dog carrying the SOD1 mutation may be outstanding in every other respect.

Responsible breeding is therefore about evaluating the whole dog, not a single DNA result.

This principle applies to all breeds and to all aspects of breeding, not just Degenerative Myelopathy.

Why breeders focus on validated health testing

This is why DNA tests that have been scientifically validated for Finnish Lapphunds are so valuable.

For conditions such as prcd-PRA and Pompe Disease, researchers have demonstrated that the mutations reliably predict inherited disease within the breed.

These tests allow breeders to make informed mating decisions that avoid producing affected puppies while still maintaining genetic diversity.

The SOD1 mutation is different.

There is currently no evidence demonstrating that eliminating all SOD1 carriers from the Finnish Lapphund breeding population would reduce the already exceptionally low incidence of Degenerative Myelopathy.

Without that evidence, removing otherwise healthy dogs from breeding solely because of their SOD1 result risks reducing genetic diversity without any demonstrated benefit to the breed.

Following the evidence

Good breeding is not about producing dogs with the greatest number of "clear" results.

Nor is it about ignoring new genetic discoveries.

Responsible breeding requires balancing many different factors, including:

DNA tests that have been scientifically validated for the breed.
Hip and elbow scores.
ACES eye examination results.
Temperament and behaviour.
Longevity within the family.
Breed type and structure.
Overall genetic diversity.

Each of these contributes to the health and future of the breed.

As scientific knowledge grows, breeding recommendations should continue to evolve. If future research demonstrates that the SOD1 mutation has meaningful clinical significance in Finnish Lapphunds, responsible breeders should adapt their breeding strategies accordingly.

Until then, the available evidence supports using validated health tests while preserving the broad genetic diversity that is essential for the long-term health of the Finnish Lapphund.

Responsible breeding has always involved balancing the best available scientific evidence with the long term health of the breed. As our understanding of Degenerative Myelopathy continues to evolve, so too should our breeding decisions. Until stronger evidence becomes available, the current evidence supports focusing on health tests that have been scientifically validated for Finnish Lapphunds while continuing to monitor future research into the SOD1 mutation.

Ultimately, the goal of responsible breeding is not to produce dogs with the longest list of "clear" DNA results.

The goal is to produce healthy dogs by making breeding decisions based on the strongest available scientific evidence.

Sometimes that means using a DNA test extensively, as with prcd-Progressive Retinal Atrophy (prcd-PRA). Sometimes it means recognising that a test has not yet been shown to provide meaningful predictive information for a particular breed.

Understanding the difference is one of the fundamental principles of evidence-based breeding.

Frequently Asked Questions

Q: My dog tested "At Risk". Should I be worried?

A: An "At Risk" result means your dog has inherited two copies of the SOD1 mutation being tested by the laboratory. It does not mean your dog has Degenerative Myelopathy, nor does it mean your dog will inevitably develop the disease.

Even in breeds where the relationship between the SOD1 mutation and Degenerative Myelopathy has been well established, many genetically "at risk" dogs never develop clinical disease.

For Finnish Lapphunds, the relationship between the SOD1 mutation and clinical Degenerative Myelopathy has not been scientifically validated. This means that, unlike validated DNA tests such as prcd-PRA, an "at risk" result cannot currently be interpreted as a reliable predictor of whether an individual Finnish Lapphund will develop the disease.

Q: Does an "At Risk" result mean my dog will develop Degenerative Myelopathy?

A: No.

A DNA result is not a diagnosis.

It identifies a genetic mutation, not whether disease is present or will occur in the future.

Current evidence indicates that additional genetic and environmental factors influence whether Degenerative Myelopathy develops.

Q: Can a dog that is genetically "clear" still develop Degenerative Myelopathy?

A: Yes.

Even in breeds where the SOD1 mutation has been validated, cases have been reported in dogs without the expected genetic result.

This is one of the reasons the SOD1 mutation is not considered fully predictive of disease.

Q: Can a veterinarian diagnose Degenerative Myelopathy from a DNA test?

A: No. A DNA test cannot diagnose Degenerative Myelopathy.

The diagnosis of Degenerative Myelopathy is based on a combination of clinical signs, neurological examination, diagnostic imaging to exclude other diseases, and the dog's history.

A definitive diagnosis generally requires microscopic examination of the spinal cord after death.

Q: Why do Embark, Orivet and other laboratories test for SOD1 if it hasn't been validated for Finnish Lapphunds?

A: Commercial DNA laboratories produce testing panels that include genetic variants from many different breeds.

The SOD1 mutation is clinically important in several breeds, so it is included in these broader testing panels.

The laboratory is accurately reporting whether the mutation is present.

There is nothing incorrect about laboratories including the SOD1 result in their reports. In fact, providing comprehensive genetic information is valuable, particularly as scientific understanding continues to evolve.

The important question is not whether the mutation is present. The important question is how that result should be interpreted for the individual breed being tested.

This is where breed specific validation becomes essential. While the SOD1 result has established clinical significance in some breeds, there is currently no published evidence demonstrating that it has the same predictive value in Finnish Lapphunds.

Q: Is the laboratory wrong?

Y: No. The laboratory is accurately identifying the SOD1 mutation.

The question is not whether the mutation exists.

The question is whether the mutation has been shown to reliably predict Degenerative Myelopathy in Finnish Lapphunds.

At present, there is no published evidence demonstrating that it does.

Q: Why do some breeders advertise "DM Clear" dogs?

A: Breeders naturally want to demonstrate that they are health testing their dogs and making informed breeding decisions.

Some breeders also choose to avoid the SOD1 mutation entirely as an additional precaution.

Others place greater emphasis on health tests that have been scientifically validated for Finnish Lapphunds while considering the SOD1 result to have limited practical significance based on the current evidence.

Neither approach changes the fact that the relationship between the SOD1 mutation and Degenerative Myelopathy has not yet been validated for Finnish Lapphunds.

Q: Should I only buy a puppy that is genetically "clear" for SOD1?

A: Evidence does not support using the SOD1 result when evaluating a Finnish Lapphund breeder or litter.

Far more important questions include:

Are the parents health tested for conditions that have been validated in the breed?
Have they undergone hip and elbow scoring?
Have they had current ACES eye examinations?
Do they have sound temperaments?
Does the breeder make balanced decisions that consider the overall health and genetic diversity of the breed?

Breeding is about evaluating the whole dog, not a single DNA result.

Q: Should breeders avoid using all SOD1 carriers?

A: There is currently no evidence that eliminating SOD1 carriers from the Finnish Lapphund breeding population would reduce the already exceptionally low incidence of Degenerative Myelopathy.

Conversely, unnecessarily removing otherwise healthy dogs from breeding may reduce genetic diversity, which is itself important for the lon -term health of the breed.

For this reason, many breeders focus their breeding decisions on health tests that have been scientifically validated for Finnish Lapphunds while continuing to monitor emerging research.

Q: Could the recommendations change in the future?

A: Absolutely. Science continually evolves.

If future research demonstrates that the SOD1 mutation has meaningful significance in Finnish Lapphunds, breeders should adapt their breeding practices to reflect that evidence.

Evidence based breeding means being willing to change when new, high quality scientific evidence becomes available.

Q: Why doesn't this work like prcd-PRA?

A: Because they are fundamentally different DNA tests.

The mutation responsible for prcd-Progressive Retinal Atrophy has been scientifically validated in Finnish Lapphunds. The relationship between the mutation and the disease is well understood, making the DNA test a reliable breeding tool.

The SOD1 mutation has not been validated for Finnish Lapphunds.

This is why responsible breeders treat these two DNA tests differently.

Q: Should I ask breeders about DM?

A: Yes, but it's worth asking the right question.

Rather than asking whether the parents DM status, ask how the breeder interprets the SOD1 result, what health testing they prioritise, and why.

A knowledgeable breeder should be able to explain the current scientific evidence, discuss why prcd-PRA and Pompe Disease are treated differently, and describe how they balance DNA testing with hip and elbow scoring, ACES eye examinations, temperament, longevity and genetic diversity.

q: What We Still Don't Know

A: One of the defining principles of good science is recognising the difference between what has been demonstrated and what remains uncertain.

Although our understanding of Degenerative Myelopathy and the SOD1 mutation has advanced considerably over the past decade, there are still many unanswered questions, particularly in Finnish Lapphunds.

At present, we do not know:

Why Degenerative Myelopathy remains exceptionally rare in Finnish Lapphunds despite the presence of the SOD1 mutation within the breed.
Whether additional modifier genes reduce or prevent the development of disease in Finnish Lapphunds.
Whether environmental or lifestyle factors influence the likelihood of disease developing.
Whether other, as yet unidentified, genetic factors contribute to Degenerative Myelopathy in the breed.
Whether there are protective genetic factors within Finnish Lapphunds that reduce the likelihood of developing clinical Degenerative Myelopathy despite the presence of the SOD1 mutation.
Whether future research will identify a stronger relationship between the SOD1 mutation and clinical disease in Finnish Lapphunds.

These unanswered questions are not unusual.

Many inherited diseases are far more genetically complex than they first appear, and our understanding often evolves as larger studies become available and new technologies emerge.

Importantly, uncertainty should not be mistaken for evidence either for or against the SOD1 mutation.

Rather, it reminds us that breeding decisions should be based on the best evidence currently available while remaining open to new discoveries as science progresses.

Conclusion

Degenerative Myelopathy is a serious neurological disease, and continued research into its causes remains important. However, the evidence currently available for Finnish Lapphunds differs markedly from that of breeds in which the relationship between the SOD1 mutation and Degenerative Myelopathy has been validated.

The SOD1 DNA test accurately identifies a genetic mutation, but there is currently no evidence demonstrating that this mutation reliably predicts Degenerative Myelopathy in Finnish Lapphunds.

Responsible breeding is not about ignoring new science, nor is it about treating every new DNA test as equally informative. It is about carefully evaluating the quality of the available evidence, understanding what each test can and cannot tell us, and making balanced decisions that protect both the health of individual dogs and the long term future of the breed.

Good science is not about pretending to have all the answers. It is about making the best decisions possible using the evidence available today, while remaining open to new evidence tomorrow.

As our understanding of Degenerative Myelopathy continues to evolve, so too should our breeding decisions. Until stronger evidence becomes available, the current evidence supports focusing on health tests that have been scientifically validated for Finnish Lapphunds while continuing to monitor future research into the SOD1 mutation.

References and Further Reading

Scientific Literature

Awano T, Johnson GS, Wade CM, et al. (2009). Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proceedings of the National Academy of Sciences, 106(8), 2794-2799.

Ivansson EL, Megquier K, Kozyrev SV, et al. (2017). Evidence of a genomic insertion in intron 2 of SOD1 causing allelic drop-out during routine diagnostic testing for canine degenerative myelopathy. Animal Genetics, 48(2), 141-148.

Zeng R, Coates JR, Johnson GC, et al. (2014). Breed distribution of SOD1 alleles previously associated with canine degenerative myelopathy. Journal of Veterinary Internal Medicine.

Veterinary and Genetics Resources

Bell JS. When 23 and Me Has Gone to the Dogs. Canine Chronicle (2019).

Beuchat C. The Lesson(s) from SOD1 and Degenerative Myelopathy. Institute of Canine Biology (2018)

Beuchat C. Why We Need a More Holistic Approach to Managing Canine Genetic Disorders. Institute of Canine Biology (2016).

Beuchat C. Why Do Dogs Have So Many Genetic Disorders? Institute of Canine Biology (2013).

Breed Specific Information

Lappalaiskoirat ry (Lapphund Club of Finland) health committee communications relating to Degenerative Myelopathy.

Mary Starling. DM and the Finnish Lapphund (2019), breed health article.

Disclaimer

This article is intended as an educational resource summarising the current scientific understanding of Degenerative Myelopathy and the SOD1 mutation in Finnish Lapphunds.

Scientific knowledge evolves over time. Readers are encouraged to consider newly published research as it becomes available and to discuss individual health concerns with their veterinarian.

Author: Lauren Mills, Orical Finnish Lapphunds, Australia

Version: Version 1.0

Published: 2026

This article may be shared in its original form for educational purposes. It should not be reproduced, edited or republished without permission. Scientific understanding evolves over time, and this document reflects the evidence available at the date of publication.