--- license: permission_granted topic_id: companion_breed_health_dutch_tulip_hound_omia4475_dog category: companion-breed-health title: "Dutch Tulip Hound — Dyskinesia, paroxysmal, SOD1-related (hereditary; OMIA-verified breed predisposition)" lang: en source: "OMIA (Online Mendelian Inheritance in Animals, University of Sydney) breed-specific hereditary-disorder record, saved verbatim to source_file; C1 substring-verified. Pulled 2026-08-02 from local OMIA database dump." source_file: pdf-raw/breed-health/dutch_tulip_hound_omia4475_4475.txt date_parsed: 2026-08-02 tokens_estimated: 398 verification: method: substring_match claims: 7 passed: 7 date: 2026-08-02 recovered: false path: companion-breed-health/companion_breed_health_dutch_tulip_hound_omia4475_dog/01_companion_breed_health_dutch_tulip_hound_omia4475_dog.md source_document: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" citation: authority: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" title: "Dutch Tulip Hound — Dyskinesia, paroxysmal, SOD1-related (hereditary; OMIA-verified breed predisposition)" url: "https://omia.org/OMIA002322/9615/" retrieved: "2026-08-02" ref: "OMIA breed-specific hereditary-disorder records (omia.org), derived from local OMIA database dump; dataset: https://doi.org/10.25910/2AMR-PV70" doc_type: "academic animal-genetics database (breed-specific disorder entries)" needs_review: false
Dutch Tulip Hound — Dyskinesia, paroxysmal, SOD1-related (hereditary; OMIA-verified breed predisposition)
Source: first-hand OMIA (University of Sydney) breed-specific hereditary-disorder record, saved verbatim to source_file; every claim below is a C1 byte-substring of it.
Claims
Breed: Dutch Tulip Hound (Dog)Disorder:Mode of inheritance: Autosomal recessiveSummary: A different mutation in the SOD1 gene causes adult onset disease: OMIA 000263-9615 : Degenerative myelopathy in Canis lupus familiarisClin feat: Mandigers et al. (2021): Affected pups exhibited clinical signs of a severe tetraparesis, dystonia, cramping and falling over when trying to walk. In most cases, the presentation deteriorated within weeks and elective euthanasia was performed. ... In all pups, routine hematology and clinical chemistry and urinalysis did not reveal any significant abnormalities. In two pups the complete vertebral column was radiographically examined, in four pups an EMG (electromyogram) performed and these did not reveal any abnormalities. On four pups a so-called tensilon test was performed that ruled out myasthenia gravis. In two pups the acetylcholinesterase receptor titer for myasthenia gravis was measured and was found not to be abnormal. In seven pups titers for toxoplasmosis and neospora revealed no increase. In three pups an additional organic acid analysis was performed, which did not reveal any abnormality.Defect: yesPathology: Mandigers et al. (2021): Routine post-mortem examinations were possible in 8 of these 12 pups. These revealed no morphological abnormalities macroscopically. Histologically, the most consistent finding was mild, random Wallerian-like degeneration in the brain stem and spinal cord with mild denervation atrophy of the skeletal muscle.
Associated gene(s)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- Gene: Entrez Gene ID 403559 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene
- OMIA molecular-genetics note: Mandigers et al. (2021): "The DNA sequence analysis of SOD1 showed that the patients were homozygous for a frameshift mutation in the fourth codon. ... A G-nucleotide of the fourth codon of the gene is replaced by a CAC-trinucleotide. The shifted coding sequence runs into a stop codon at the tenth codon. The annotation of the indel mutation is NM001003035.1:c.12delinsCAC. The protein annotation is…
Evidence (references)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- 2021. A knockout mutation associated with juvenile paroxysmal dyskinesia in Markiesje dogs indicates SOD1 pleiotropy. Hum Genet — PubMed:PMID33677640 | DOI:10.1007/s00439-021-02271-6 — OMIA Phene_Article / Article
- 2021. International veterinary canine dyskinesia task force ECVN consensus statement: Terminology and classification. J Vet Intern Med — PubMed:PMID33769611 | DOI:10.1111/jvim.16108 — OMIA Phene_Article / Article
- 2021. Nearly 30 years of animal models to study amyotrophic lateral sclerosis: A historical overview and future perspectives. Int J Mol Sci — PubMed:PMID34830115 | DOI:10.3390/ijms222212236 — OMIA Phene_Article / Article
- 2022. Dystonia in veterinary neurology. J Vet Intern Med — PubMed:PMID36086931 | DOI:10.1111/jvim.16532 — OMIA Phene_Article / Article
- 2024. Canine paroxysmal dyskinesia-a review. Front Vet Sci — PubMed:PMID39119350 | DOI:10.3389/fvets.2024.1441332 — OMIA Phene_Article / Article
- 2023. An overview of canine inherited neurological disorders with known causal variants. Animals (Basel) — PubMed:PMID38003185 | DOI:10.3390/ani13223568 — OMIA Phene_Article / Article
Comparative medicine (human OMIM)
Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.
- OMIM:147450 (type: gene) — OMIA Group_OMIM (via OMIA_ID)
- OMIM:618598 (type: trait) — OMIA Group_OMIM (via OMIA_ID)
- OMIM:105400 (type: trait) — OMIA Group_OMIM (via OMIA_ID)
verification_derived: method: derived_from_dataset source: "OMIA database dump (omia.xml, local); fields Gene/Variant/Article/OMIM" note: "Structured fields (gene, variant rsID/protein change, PubMed/DOI references, OMIM cross-link) extracted from OMIA dump and presented with first-hand values; not verbatim prose."