Open-Angle Glaucoma in Beagles: 50 Years of Research and ADAMTS10

SamOur two-year-old Beagle’s eyes look fine. Why does her breeder keep bringing up glaucoma?

Elena MarshBecause researchers have followed glaucoma in Beagles for decades. A 2019 review in Veterinary Ophthalmology put it bluntly: there is no cure, and many affected dogs go blind.

SamHer DNA report has a line about ADAMTS10. Is that something real or just lab jargon?

Elena MarshIt is real and well studied. Vanderbilt researchers described the Beagle variant in PLoS Genetics in 2011, and what it means depends on how many copies she carries.

SamSo if her result says clear, can I stop thinking about her eyes altogether?

Elena MarshNot quite. A 2017 Veterinary Pathology review stressed that glaucoma variants differ between breeds, so one result answers one narrow question.

Bottom line: Primary open-angle glaucoma (POAG) in Beagles is caused by a single change in the ADAMTS10 gene, G661R, identified in 2011 by a Vanderbilt-led team working with a Beagle colony kept at the University of Florida since 1972. It is autosomal recessive: dogs with two copies develop slowly rising eye pressure, which in that colony began at 8 to 16 months of age, while one-copy carriers do not develop the disease. In small US samples the variant’s allele frequency was roughly 1 to 3%. A DNA result is risk and breeding information, not a diagnosis; only a veterinarian measuring eye pressure and examining the drainage angle and optic nerve can diagnose glaucoma. A clear result does not mean a Beagle can never get glaucoma, because angle-closure and secondary glaucoma are not covered by this test. A suddenly red, painful or cloudy eye needs a vet the same day.

A glaucoma that begins with the drain still open

Most people picture glaucoma in dogs as an emergency: one eye turns red, the pupil goes wide, the dog squints. That picture fits primary angle-closure glaucoma (PACG), a large share of canine cases, in which the drainage angle at the edge of the iris is malformed or narrow and pressure rises suddenly and severely. The American Cocker Spaniel is a typical predisposed breed, and a 2022 study in Scientific Reports found no single gene behind its form; the shape of the eye itself, including a narrow angle, appeared to set up the risk.

The Beagle form is different. K. N. Gelatt and colleagues described it in 1977 after following 55 Beagles with inherited glaucoma, splitting it into early (6 to 12 months of age), moderate (13 to 30 months) and advanced (31 months and older) stages. In the early stage, gonioscopy, the lens-on-the-eye exam that lets a vet look into the drainage angle, showed an open, normal-looking angle even though pressure was already raised and fluid was leaving the eye more slowly. Only later did the optic nerve head cup, the fibres holding the lens give way and the angle narrow. In the advanced stage the lens could dislocate and the optic nerve wasted.

That sequence explains why the disease is easy to miss: slowly rising pressure in a quiet-looking eye produces no dramatic signs. The 2013 Vanderbilt-led screening paper noted that, in clinics, “nearly all dogs present at late stages of the disease and most often suffer from significant vision loss”. A 2024 study by Pumphrey, Komáromy and colleagues added a biochemical twist: aqueous humor from dogs with chronic angle-closure glaucoma behaved differently from that of ADAMTS10 Beagles, and the authors concluded the two diseases may arise by different mechanisms.

The Beagle ranked No. 7 in the American Kennel Club’s 2025 registration list, so even a rare variant touches many households.

SamIf the angle looks normal, how would anyone know my Beagle’s pressure is creeping up?

Elena MarshOnly by measuring it. In Gelatt’s 1977 study of 55 colony Beagles, pressure was already raised in the early stage while gonioscopy still showed an open, normal-looking angle.

A colony founded in Florida in 1972: how the disease became visible

Science knows so much about this breed-specific glaucoma because of one research colony. The 2011 genetics paper describes “a colony of Beagle dogs established in 1972, which is a well-characterized and naturally occurring animal model of POAG”. Gelatt, of the University of Florida, co-authored that paper and much of the earlier work, including a 1981 American Journal of Pathology report on “inherited primary open angle glaucoma in the beagle”. The appeal was a dog that develops open-angle disease on its own rather than having it induced.

Long-term follow-up showed how gradual the disease is. In 2003 Gelatt’s group tracked 13 untreated glaucomatous Beagles for four years with color Doppler imaging. Average eye pressure was 19.4 mmHg in early disease, still inside the normal range, then 29.7 mmHg in the moderate stage and 44.5 mmHg in the advanced stage. Blood-flow changes were already present before pressure crossed the normal limit.

Multigeneration breeding in the colony settled the inheritance: autosomal recessive, analysed in 2011 as “autosomal recessive with 100% penetrance” within the colony. The gene stayed unknown for almost four decades. Two obvious candidates were dropped in 2009, when University of Tokyo researchers working with Gelatt reported that neither MYOC nor CYP1B1 explained the Beagle disease.

Population data put the colony in context. Gelatt and MacKay’s 2004 survey of North American university clinic records found primary glaucoma of any type in 0.89% of purebred dogs seen in 1994 to 2002, led by the American Cocker Spaniel (5.52%) and Basset Hound (5.44%); the Beagle was not in the top ten. An older study of dogs hospitalized in 1979 to 1983 listed the Beagle among eight breeds at higher risk than mixed breeds. Neither figure separates open-angle from angle-closure disease, so neither tells you how common the ADAMTS10 form is.

From 2,692 candidates to one glycine: the Vanderbilt mapping

In 2011 J. Kuchtey, R. W. Kuchtey and colleagues at the Vanderbilt Eye Institute published the answer in PLoS Genetics. They genotyped 19 affected and 10 carrier colony dogs and narrowed the disease to a 4 Mb stretch of dog chromosome 20, a region corresponding to part of human chromosome 19 linked to variation in eye pressure.

Sequencing turned up 2,692 variants that travelled with the disease; only eight changed a protein. The strongest candidate was a glycine-to-arginine swap at position 661 of ADAMTS10, written Gly661Arg or G661R, in exon 17. That glycine is conserved across 38 vertebrate species. ADAMTS10 protein turned out to be preferentially expressed in the trabecular meshwork, the tissue that drains fluid from the eye, and in a test-tube experiment in aqueous humor the mutant protein broke down faster, with a half-life of 255.8 minutes against 636.9 minutes, roughly 40%. The authors also noted that a definitive diagnosis in the colony “cannot be made until two years of age”, and that the colony Beagles had no problems outside the eye.

The 2013 follow-up in Investigative Ophthalmology & Visual Science screened Beagles from two supplier colonies plus dogs seen in veterinary hospitals. G661R was the only candidate consistent with glaucoma in the general Beagle population, and the only homozygous dog outside the colony was an unrelated pet Beagle examined at five years old with open angles and raised pressure in both eyes. G661R was absent from 43 glaucomatous dogs of other breeds, including 26 American Cocker Spaniels and 7 Basset Hounds; the authors concluded that primary glaucoma in dogs “is likely to be genetically complex”.

SamDoes one swapped amino acid really explain a whole disease?

Elena MarshIn this breed it appears to. Vanderbilt’s 2013 screen found G661R was the only variant matching glaucoma in pet Beagles, and it was absent from 43 dogs of other breeds.

What a dog gene changed in human glaucoma research

ADAMTS10 is a secreted enzyme that binds fibrillin-1 microfibrils, thread-like structures that give tissues elasticity, and helps them form. In 2014 the Kuchteys used the dog finding to propose the “microfibril hypothesis of glaucoma”: defective microfibrils could be a root cause of raised eye pressure. They noted that two other human glaucoma genes, LOXL1 (exfoliation glaucoma) and LTBP2 (congenital glaucoma), are also tied to microfibrils, which help control TGFβ signalling, and floated the idea that approaches used against chronic TGFβ activation in Marfan syndrome might one day apply to glaucoma. That remains a hypothesis, not a treatment for dogs.

Moving the Beagle variant into mice gave a surprise. In 2021, mice carrying G661R did not develop raised eye pressure; they were smaller, with thicker corneas and shallower front chambers. A 2022 Matrix Biology study then found weaker retinal ganglion cell function, thinner optic nerves with fewer axons and lower TGFβ signalling during development. For the pressure side of the disease, the dog remains the key model.

In people, two faulty copies of ADAMTS10 cause autosomal recessive Weill-Marchesani syndrome, described in 2004 as short stature, short fingers, stiff joints and lens problems; a 2024 review found ADAMTS10 variants in 19 of 61 patients. The colony Beagles had none of the body-wide features. Same gene, different disease.

Softer sclera, slower vision loss: the biomechanics studies

One distinctive finding concerns the sclera, the tough white wall of the eye through which the optic nerve exits. In 2013 Palko and colleagues found the posterior sclera of G661R dogs significantly less stiff than in age-matched controls (P<0.001), with less insoluble collagen, the two tracking closely (R=0.88). They described it as inherently weaker “before clinical indications of optic nerve damage”. A 2016 synchrotron X-ray study of three affected dogs and three age-matched carriers found lower collagen density, and another 2016 study of 10 mutant and 5 normal dogs showed the sclera stiffens with age at a similar rate in both groups but stays softer in mutants (p=0.041).

A 2021 review by Park and Komáromy drew the clinical conclusion: “Vision loss progresses much more slowly in Beagles with open-angle glaucoma (OAG) caused by ADAMTS10 mutation”, probably because of these biomechanical changes, which they regarded as a property of the variant rather than a consequence of pressure.

Michigan State University’s 2023 study added another measurement. In 39 dogs with the variant and 14 controls, average eye pressure was 23.0 mmHg against 15.3 mmHg, and ocular pulse amplitude, the small pressure swing with each heartbeat, was lower in affected dogs (4.1 vs 6.5 mmHg). These dogs, the authors wrote, “tolerate elevated IOP much better, with slower progression of vision loss, than other glaucoma-affected breeds with comparable IOPs”. One detail is easy to get wrong: a 2024 paper from the same programme describes its colony as “Beagle-derived mongrel dogs carrying the G661R missense mutation”, not purebred Beagles.

“Slower” is relative. It means more time between diagnosis and serious vision loss than in many glaucomatous breeds, not a mild disease.

SamDoes slower mean my Beagle could keep her sight for life if she has two copies?

Elena MarshNobody can promise that. Park and Komáromy’s 2021 review says vision loss is much slower than in other breeds, but no study has shown how long sight lasts in a pet Beagle.

The eye drops tested in these Beagles

A genetically defined model is a natural test bed for glaucoma medicines, and the results have been sobering. In a 2021 trial in five normal and five ADAMTS10 Beagles, netarsudil, a newer human glaucoma drop, lowered pressure only slightly, an effect the authors judged clinically irrelevant, and it reddened the conjunctiva. A second 2021 study compared a netarsudil-latanoprost combination with latanoprost alone: both lowered pressure, with no difference between them. These short studies in research dogs are described to show what has been tried, not to suggest any drug for a pet; treatment choices belong to your veterinarian or a veterinary ophthalmologist.

The wider picture comes from a 2019 paper on the future of canine glaucoma therapy with 14 authors: “there is no cure, and many affected dogs go blind”. Uncontrolled pressure is painful, and removal of the eye is often the outcome. A 2021 review by Park and Komáromy adds that reducing eye pressure is the only treatment proven to delay progression. A 1986 study found that in predisposed breeds, preventive treatment of the second eye lengthened the time until it too was affected. No study has shown that starting treatment early in an ADAMTS10 Beagle changes long-term vision. The 2019 authors looked ahead to DNA tests that flag inherited glaucoma years before signs appear, the role the G661R test now partly fills.

Reading a G661R result without overreading it

A dog with no copies is clear. A dog with one copy is a carrier: under autosomal recessive inheritance it is not expected to develop this form of glaucoma, but it can pass the variant on. A dog with two copies is at high risk and should have eye pressure checks on a plan agreed with your vet.

How common is the variant? Nobody has measured it in today’s pet Beagles. The 2011 study found one carrier among 48 unrelated, unaffected Beagles, an allele frequency of about 1%; the 2013 study found 3.1% in a hospital sample, again based on one carrier. These are small US samples, and an allele frequency is not a carrier rate. The 2013 authors calculated that if roughly 1% of Beagles have primary glaucoma, the allele frequency should not exceed 10%.

Three limits matter. First, a clear Beagle can still develop angle-closure glaucoma or secondary glaucoma from inflammation, a dislocated lens, a tumour or injury. Second, results do not transfer between breeds. The Norwegian Elkhound has its own ADAMTS10 variant, A387T, reported by the University of Helsinki in 2014, with roughly one in four Elkhounds in a five-country sample carrying it; Basset Hounds, the Basset Fauve de Bretagne and the Petit Basset Griffon Vendéen have open-angle glaucoma caused by a different gene, ADAMTS17. Japanese researchers likewise found no G661R in 98 Shiba Inu or 67 Shih Tzu. Third, a gene says nothing about the pressure in a particular eye today. A 2017 Veterinary Pathology review concluded that because variants differ between and within breeds, gene discoveries have limited value as a general screen, and no ideal biomarker for early diagnosis yet exists.

SamMy Beagle is a carrier. Should I worry about her own eyes?

Elena MarshCarriers are not expected to develop this recessive form. Michigan State’s 2023 study used carriers alongside normal dogs as controls. Routine eye checks still apply.

Ordering the test in the US and UK, and what breed bodies ask for

Lab coverage for the Beagle variant is patchy, so check the exact wording before you pay. Prices were read on 9 October 2026; sale prices change.

• Wisdom Panel has a condition page that names ADAMTS10 on chromosome 20 and credits the 2011 Kuchtey paper, the Beagle variant. Premium had a list price of $159.99 in the US and £144.99 in the UK as of 2026-10-09 (often discounted; check the current price). But the Premium product pages list POAG only for the Basset Fauve de Bretagne, Petit Basset Griffon Vendéen and Shar-Pei (ADAMTS17 types), so we could not confirm the Beagle variant is in the consumer kit. Ask before ordering.
• LABOKLIN UK lists test 8452 at £48.00 including 20% VAT (January 2026 catalogue), one to three weeks, cheek swab or EDTA blood. The same code covers Beagles, Norwegian Elkhounds and the ADAMTS17 breeds. Its non-Kennel-Club Beagle bundle (8620, £138.00) includes POAG; the Kennel Club Beagle bundle (8701, £126.00) does not. LABOKLIN marks the Norwegian Elkhound as part of the Kennel Club DNA testing scheme for this test but not the Beagle, so a Beagle POAG result is not recorded with the Royal Kennel Club.
• Genomia, a Czech lab that ships internationally, names c.1981G>A (p.Gly661Arg) and charges $56.00 excluding VAT, usually in 12 business days.
• Embark‘s glaucoma condition page showed only the Norwegian Elkhound variant; we could not verify that it reports the Beagle variant.

Neither the US nor the UK currently asks Beagle breeders for this test. The AKC parent-club recommendations for the Beagle are hips, cardiac exam, ophthalmologist evaluation, thyroid and the MLS DNA test, and the National Beagle Club of America’s CHIC list matches, with no POAG test. The Orthopedic Foundation for Animals has no POAG test on its OFA/University of Missouri list ($65 per test), but outside lab results can be registered for $15.

In the UK, the Royal Kennel Club’s Beagle page lists Lafora’s and NCCD tests as good practice and FVIID, IGS-2 and MLS as best practice, with no POAG test. By contrast it lists a POAG DNA test as minimum good practice for the Norwegian Elkhound, noting in 2020 that “there is no means of clinically screening for POAG”. Licensed breeders in England also work under the Animal Welfare (Licensing of Activities Involving Animals) (England) Regulations 2018, which cover anyone breeding three or more litters in 12 months and bar keeping a dog for breeding if, on the basis of its genotype, phenotype or health, breeding could harm its own or its puppies’ welfare. Wisdom Panel’s breeder notes state that carrier-to-carrier matings are not advised because the litter may contain affected puppies.

From your regular vet to an ophthalmologist, and where insurance fits

A DNA result starts a conversation with your veterinarian. A two-copy Beagle needs regular tonometry (eye pressure measurement), and your vet may refer you to a board-certified veterinary ophthalmologist; in the US the American College of Veterinary Ophthalmologists (ACVO) offers a “Find Ophthalmologist” search.

One trap catches many owners. An OFA Companion Animal Eye Registry (CAER) exam, performed by ACVO diplomates and registered for $15, is a screening exam. The OFA itself states that it does not include measuring intraocular pressure and that “dogs with goniodysgenesis, glaucoma … might not be detected without further testing”. An eye clearance therefore does not rule out ADAMTS10 glaucoma in a young Beagle whose angle still looks open.

In the UK, the BVA/RKC/ISDS Eye Scheme’s panel of 42 ophthalmologists charges £72.00 per dog including VAT (from 1 January 2026) for a routine eye examination, a gonioscopy or a POAG examination. Its 2026 list of known inherited eye diseases certifies POAG for the Basset Hound, Petit Basset Griffon Vendéen and Shar-Pei but does not list the Beagle, so British Beagles rely on DNA testing and vet monitoring.

Insurance timing matters more than the gene. Embrace (US) covers hereditary conditions “when not pre-existing at the time of enrollment”; Nationwide excludes pre-existing conditions. In the UK, Agria treats hereditary conditions as pre-existing if signs appeared or a diagnosis was made before cover began, and Petplan covers hereditary conditions “that haven’t shown symptoms before the start of your policy”, with Covered for Life limits of £4,000, £7,000 or £12,000 a year. None of these pages says how a positive DNA result without symptoms is treated, so ask in writing and insure early.

Some signs cannot wait for a scheduled check: an eye that is suddenly red, painful, cloudy or bulging, a pupil that stays wide, or squinting. Glaucoma can cost a dog its sight, so see a vet the same day.

SamHer CAER exam came back clear last spring. Doesn’t that already rule glaucoma out?

Elena MarshNo. The OFA says its certification exam does not measure eye pressure, and Gelatt’s 1977 Beagles had normal-looking angles early on. The two checks answer different questions.

Frequently asked questions

Q. Can a DNA test diagnose glaucoma in my Beagle?
No. The test shows whether your dog carries zero, one or two copies of the G661R variant in ADAMTS10. Glaucoma is diagnosed by a veterinarian measuring eye pressure and examining the drainage angle and optic nerve. In the Florida colony, a definitive diagnosis could not be made before about two years of age.

Q. My Beagle is clear. Can she still get glaucoma?
Yes. A clear result rules out this one inherited form only. Angle-closure glaucoma and secondary glaucoma from inflammation, lens problems, tumours or injury are not detected by this test, so routine eye checks still matter.

Q. Will a carrier Beagle develop glaucoma?
Carriers have one copy, and this form of glaucoma is autosomal recessive, so they are not expected to develop it. They can pass the variant to puppies, which matters for breeding decisions.

Q. At what age does ADAMTS10 glaucoma start?
In the University of Florida research colony, eye pressure began to rise at 8 to 16 months. Owners usually notice much later; Wisdom Panel’s veterinary notes say first clinical signs are typically seen at 2 to 5 years, and an affected pet Beagle in the 2013 study was examined at five years old.

Q. Is there a cure?
No. A 2019 specialist review states there is no cure for canine glaucoma; a 2021 review notes that lowering eye pressure is the only treatment proven to delay progression. Treatment decisions belong to your veterinarian or a veterinary ophthalmologist.

Q. Does the Beagle test work for Norwegian Elkhounds or Basset Hounds?
No. The Elkhound has a different ADAMTS10 variant (A387T), and Basset-type breeds have open-angle glaucoma caused by ADAMTS17. Each breed needs the test for its own variant.

Q. Do US or UK breed clubs require this test for Beagles?
Not at present. The AKC and National Beagle Club of America recommendations and the Royal Kennel Club’s Beagle health section do not include a POAG DNA test, although the Kennel Club does recommend one for Norwegian Elkhounds.

References

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About the author

Elena Marsh

Editor & writer (not a veterinarian)

A writer with a molecular-biology background and a lifelong dog and cat owner. Not a veterinarian — she translates peer-reviewed genetics research and primary data into plain language, always as information rather than diagnosis.