Airedale Terrier
Airedale Terriers have a cited life expectancy of 12 years (McMillan 2024 / VetCompass, n=1,270, 95% CI 11.8 to 12.3). The most carried tested variant is Protein Losing Nephropathy, in 16% of 200 Airedale Terriers tested (Donner 2023), then Degenerative Myelopathy (13%) and Hyperuricosuria (4%). Only 18 dogs stand behind the atlas figures here, so little is known yet.
Also known as Airedale, Bingley Terrier, King of Terriers, and Waterside Terrier.
What genetic diseases do Airedale Terriers carry?
From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Airedale Terriers carry 6 of them at observable frequency. Carrier frequency is not clinical risk. Most recessive variants require two copies for disease expression; many dominant variants show incomplete penetrance. Read this as a population fingerprint of what's in the gene pool, not a per-dog prediction.
NPHS1what this gene does
NPHS1 is a gene important for kidney function, helping to keep proteins in the blood where they belong.
For your dog: If your dog’s breed is on the list, it’s worth asking your vet about NPHS1 to understand any risks and keep an eye on kidney health.
SOD1what this gene does
SOD1 is a gene that helps protect cells from damage caused by harmful molecules called free radicals.
For your dog: If your dog is a carrier of SOD1 variants, it's worth discussing with your vet, but remember carrier status doesn't mean your dog will get the disease.
SLC2A9what this gene does
SLC2A9 is a gene that helps regulate uric acid levels in a dog's body. It plays a role in how the kidneys handle this substance.
For your dog: If your dog is one of the breeds known to carry this gene variant, it’s worth discussing with your vet to understand any potential urinary health concerns.
RPGRIP1what this gene does
RPGRIP1 is a gene involved in the function of photoreceptor cells in the eye, which help dogs see in different light conditions.
For your dog: If your dog belongs to a breed known to carry RPGRIP1 mutations, it’s worth discussing with your vet to understand the risks and monitor eye health.
What these results mean for a Airedale Terrier
12.8% of Airedale Terriers in the Donner 2023 cohort carried it (n=200).
- DM is a loss of function in the spinal cord that begins in adulthood and progresses to paralysis of the back legs. There is no treatment that stops it.
OMIA 000263-9615
“This is an adult onset degeneration of the spinal cord that progresses to paraplegia and tetraparesis. There is no successful treatment. A genetic test is available.” OMIA 000263-9615
- Two copies of the SOD1 variant mean at risk, not affected. Some dogs with two copies never show signs.
OMIA 000263-9615
“some homozygous mutant dogs had no signs of degenerative myelopathy, which suggests incomplete penetrance or other causative loci” OMIA 000263-9615
- One copy makes a dog a carrier. In the study that found the variant, every affected dog tested had two copies.
OMIA 000263-9615
“All affected dogs tested were homozygous mutant.” OMIA 000263-9615
What to do
A DNA result is not a diagnosis. Take the result, and any change in how the dog walks, to a veterinarian.
No test, or a mix
Without a test nobody can say how many copies a dog has. A breed's carrier frequency describes the breed, not this dog.
Other names
The Airedale Terrier is also recorded as Airedale, Bingley Terrier, King of Terriers, and Waterside Terrier.
Identified as Airedale Terrier (VBO:0200008) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 7 · iDog 3 · VeNom 14929.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Airedale Terrier
In the atlas, the Airedale Terrier clusters consistently as Airedale Terrier (100% of the 18 dogs here). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.
Only 18 dogs of this breed in the atlas, modestly sampled.
What the atlas genotypes say about Airedale Terrier
Computed from the 14,478 CanVAS dogs in the Atlas, on an imputed genotype backbone: 77,215 directly typed sites per dog, imputed to 9.67 million variants.
The confidence below counts dogs, not reads: it is the size of the sample, and it is separate from how the genotypes were measured.
Not enough dogs in the atlas yet (n=18) for a reliable diversity figure. It fills in as more are added.
What does genetic diversity mean?
How varied a breed's gene pool is — the share of gene spots where a typical dog of the breed carries two different versions rather than two identical ones.
How to read it: Higher = more diverse. Among well-sampled breeds it ranges roughly 0.22 (least diverse) to 0.33 (most diverse).
Diversity is a strength, not a verdict on any individual dog. Lower diversity means it's worth paying attention to recessive-risk testing — not that a dog is doomed.
Not enough dogs in the atlas yet (n=18) to resolve cluster structure. It fills in as more are added.
What does within-breed variation mean?
How much individual dogs within the breed differ from each other genetically.
How to read it: Higher = more internal variety among individuals of the breed.
Sensitive to how many dogs of the breed we've sampled.
What does typical lifespan mean?
The median age dogs of the breed tend to reach.
How to read it: Higher = longer-lived. Compare to longevity-for-size to see whether it's just a size effect.
Drawn from population lifespan records; individual dogs vary widely with care, genetics, and luck.
Airedale Terriers are a natural model for human disease
Because the same genes cause the same conditions across species, the inherited conditions documented in Airedale Terriers help researchers understand, and work toward treating, the human diseases they model. This is the dog advancing human medicine. The breed models the human disease; it does not have it, and this is not a prediction for your dog.
- hemophilia B, modeled by the breed's Haemophilia B via F9, the same underlying biology.
- narcolepsy 1, modeled by the breed's Narcolepsy via HCRTR2, the same underlying biology.
- Caffey disease, modeled by the breed's Craniomandibular osteopathy, generic , the same underlying biology.
- congenital factor VII deficiency, modeled by the breed's Factor VII deficiency , the same underlying biology.
- OMIM:605883, modeled by the breed's Surfactant metabolism dysfunction, pulmonary , the same underlying biology.
Every condition recorded in the Airedale Terrier
Beyond the testable carriers above, OMIA's literature catalogue records 5 genetic conditions in the Airedale Terrier, 5 of which have a known human equivalent. This is the documented landscape across all Airedale Terriers ever studied, not a prediction for any one dog.
- Haemophilia B X-linked recessiveHuman equivalent: hemophilia B
- Narcolepsy Autosomal recessiveHuman equivalent: narcolepsy 1
- Craniomandibular osteopathy, generic MultifactorialHuman equivalent: Caffey disease
- Factor VII deficiency Autosomal recessiveHuman equivalent: congenital factor VII deficiency
- Surfactant metabolism dysfunction, pulmonary Autosomal recessive lethalHuman equivalent: OMIM:605883
Where every number on this page came from.
This page draws on three primary data sources. Carrier frequencies for the Mendelian section come from Donner et al. 2023 (CC-BY-4.0). We grade these data at evidence Limited because the cohort is a direct-to-consumer ascertainment, which biases toward owners who chose to test their dogs. The panel also uses tag-SNP proxies for some variants rather than direct causal-variant assays. Limited is a study-design grade, not a quality grade: the Donner cohort is the largest open canine-genotype dataset in existence and we are grateful for it. We rate the confounding MEDIUM.
Population-genetic dimensions (heterozygosity, intra-breed PCA distance, nearest neighbors, trait-locus frequencies) come from CanVAS (Brundage 2026), harmonized through the Sniff Atlas. The exact release date and verification commit are pinned at the bottom of the page so a researcher can trace a number back to a specific snapshot. The disease-gene-variant graph comes from OMIA (Online Mendelian Inheritance in Animals; Nicholas, Tammen, and the Sydney Informatics Hub at the Sydney School of Veterinary Science, The University of Sydney; retrieved April 2026, DOI 10.25910/2AMR-PV70).
What this page does not yet have. Inheritance modes and per-disease penetrance evidence from Donner 2023 are in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references live on the gene and disease pages this page links to, rather than being repeated here. What is still absent from this breed page is anything not in the cited panel, and each such gap carries its cause where it appears.
How to cite this page. The computed dimensions on this page are derived from the open Sniff Atlas v1.0.1 (Gehring 2026, doi:10.5281/zenodo.20566358, CC-BY 4.0). Full citation formats including BibTeX, RIS, and CITATION.cff at sniff.world/cite.
Some things about living with a airedale terrier never make it into a database. Add what you know as a Keeper, in your words →
Lived experience, kept beside the science.We have 18 airedale terriers. We do not have yours.
We can already place this breed on the atlas. We hold genetic diversity for n=18 of this breed in the atlas. Our floor for showing a cited rate is n=20. That is 2 more of this breed in our atlas, not in a published study.
Adding your dog is 1 of those 2 in the Sniff atlas cohort. Adding them is free and permanent.
Enrollment is free. The data stays open. The star is permanent.
- Donner J, Freyer J, Davison S, Anderson H, Blades M, Honkanen L, et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651. doi:10.1371/journal.pgen.1010651
- Brundage DM (2026). CanVAS: A Harmonized and Imputed Canine Variant Atlas. bioRxiv. doi:10.64898/2026.04.13.718238
- Nicholas, F.W., Tammen, I., & Sydney Informatics Hub. (2026). Online Mendelian Inheritance in Animals (OMIA) [dataset]. The University of Sydney. https://omia.org. doi:10.25910/2AMR-PV70 (retrieved April 2026).