A novel form of progressive retinal atrophy in Swedish vallhund dogs
Inherited retinal degenerations, such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD), represent leading causes of incurable blindness in humans. This is also true in dogs, where the term progressive retinal atrophy (PRA) is used to describe inherited photoreceptor degenerati...
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Published in | PloS one Vol. 9; no. 9; p. e106610 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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08.09.2014
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Abstract | Inherited retinal degenerations, such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD), represent leading causes of incurable blindness in humans. This is also true in dogs, where the term progressive retinal atrophy (PRA) is used to describe inherited photoreceptor degeneration resulting in progressive vision loss. Because of the similarities in ocular anatomy, including the presence of a cone photoreceptor-rich central retinal region, and the close genotype-phenotype correlation, canine models contribute significantly to the understanding of retinal disease mechanisms and the development of new therapies. The screening of the pure-bred dog population for new forms of PRA represents an important strategy to establish new large animal models. By examining 324 dogs of the Swedish vallhund breed in seven countries and across three continents, we were able to describe a new and unique form of PRA characterized by the multifocal appearance of red and brown discoloration of the tapetal fundus followed over time by thinning of the retina. We propose three stages of the disease based on the appearance of the ocular fundus and associated visual deficits. Electroretinography revealed a gradual loss of both rod and cone photoreceptor-mediated function in Stages 2 and 3 of the disease. In the few dogs that suffered from pronounced vision loss, night-blindness occurred first in late Stage 2, followed by decreased day-vision in Stage 3. Histologic examinations confirmed the loss of photoreceptor cells at Stage 3, which was associated with the accumulation of autofluorescent material in the adjacent retinal pigment epithelium. Pedigree analysis was suggestive of an autosomal-recessive mode of inheritance. Mutations in six known canine retinal degeneration genes as well as hypovitaminosis E were excluded as causes of the disease. The observed variability in the age of disease onset and rate of progression suggest the presence of genetic and/or environmental disease modifiers. |
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AbstractList | Inherited retinal degenerations, such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD), represent leading causes of incurable blindness in humans. This is also true in dogs, where the term progressive retinal atrophy (PRA) is used to describe inherited photoreceptor degeneration resulting in progressive vision loss. Because of the similarities in ocular anatomy, including the presence of a cone photoreceptor-rich central retinal region, and the close genotype-phenotype correlation, canine models contribute significantly to the understanding of retinal disease mechanisms and the development of new therapies. The screening of the pure-bred dog population for new forms of PRA represents an important strategy to establish new large animal models. By examining 324 dogs of the Swedish vallhund breed in seven countries and across three continents, we were able to describe a new and unique form of PRA characterized by the multifocal appearance of red and brown discoloration of the tapetal fundus followed over time by thinning of the retina. We propose three stages of the disease based on the appearance of the ocular fundus and associated visual deficits. Electroretinography revealed a gradual loss of both rod and cone photoreceptor-mediated function in Stages 2 and 3 of the disease. In the few dogs that suffered from pronounced vision loss, night-blindness occurred first in late Stage 2, followed by decreased day-vision in Stage 3. Histologic examinations confirmed the loss of photoreceptor cells at Stage 3, which was associated with the accumulation of autofluorescent material in the adjacent retinal pigment epithelium. Pedigree analysis was suggestive of an autosomal-recessive mode of inheritance. Mutations in six known canine retinal degeneration genes as well as hypovitaminosis E were excluded as causes of the disease. The observed variability in the age of disease onset and rate of progression suggest the presence of genetic and/or environmental disease modifiers. Inherited retinal degenerations, such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD), represent leading causes of incurable blindness in humans. This is also true in dogs, where the term progressive retinal atrophy (PRA) is used to describe inherited photoreceptor degeneration resulting in progressive vision loss. Because of the similarities in ocular anatomy, including the presence of a cone photoreceptor-rich central retinal region, and the close genotype-phenotype correlation, canine models contribute significantly to the understanding of retinal disease mechanisms and the development of new therapies. The screening of the pure-bred dog population for new forms of PRA represents an important strategy to establish new large animal models. By examining 324 dogs of the Swedish vallhund breed in seven countries and across three continents, we were able to describe a new and unique form of PRA characterized by the multifocal appearance of red and brown discoloration of the tapetal fundus followed over time by thinning of the retina. We propose three stages of the disease based on the appearance of the ocular fundus and associated visual deficits. Electroretinography revealed a gradual loss of both rod and cone photoreceptor-mediated function in Stages 2 and 3 of the disease. In the few dogs that suffered from pronounced vision loss, night-blindness occurred first in late Stage 2 , followed by decreased day-vision in Stage 3 . Histologic examinations confirmed the loss of photoreceptor cells at Stage 3 , which was associated with the accumulation of autofluorescent material in the adjacent retinal pigment epithelium. Pedigree analysis was suggestive of an autosomal-recessive mode of inheritance. Mutations in six known canine retinal degeneration genes as well as hypovitaminosis E were excluded as causes of the disease. The observed variability in the age of disease onset and rate of progression suggest the presence of genetic and/or environmental disease modifiers. |
Author | Rowlan, Jessica S Vanhapelto, Päivi Ahonen, Saija Duncan, Alison Komáromy, András M Seppälä, Eija H Cooper, Ann E Lohi, Hannes |
AuthorAffiliation | 4 Department of Veterinary Biosciences and Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland and the Folkhälsan Institute of Genetics, Helsinki, Finland 1 Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America 6 Veterinary Clinic Vetset, Kirkkonummi, Finland 3 Gavin Herbert Eye Institute, Ophthalmology Research, University of California Irvine, Irvine, California, United States of America 5 Department of Ophthalmology, University of Washington Medical School, Seattle, Washington, United States of America 2 Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America Justus-Liebig-University Giessen, Germany |
AuthorAffiliation_xml | – name: 4 Department of Veterinary Biosciences and Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland and the Folkhälsan Institute of Genetics, Helsinki, Finland – name: 1 Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America – name: 2 Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America – name: 6 Veterinary Clinic Vetset, Kirkkonummi, Finland – name: 3 Gavin Herbert Eye Institute, Ophthalmology Research, University of California Irvine, Irvine, California, United States of America – name: Justus-Liebig-University Giessen, Germany – name: 5 Department of Ophthalmology, University of Washington Medical School, Seattle, Washington, United States of America |
Author_xml | – sequence: 1 givenname: Ann E surname: Cooper fullname: Cooper, Ann E organization: Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America; Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America; Gavin Herbert Eye Institute, Ophthalmology Research, University of California Irvine, Irvine, California, United States of America – sequence: 2 givenname: Saija surname: Ahonen fullname: Ahonen, Saija organization: Department of Veterinary Biosciences and Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland and the Folkhälsan Institute of Genetics, Helsinki, Finland – sequence: 3 givenname: Jessica S surname: Rowlan fullname: Rowlan, Jessica S organization: Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America; Department of Ophthalmology, University of Washington Medical School, Seattle, Washington, United States of America – sequence: 4 givenname: Alison surname: Duncan fullname: Duncan, Alison organization: Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America – sequence: 5 givenname: Eija H surname: Seppälä fullname: Seppälä, Eija H organization: Department of Veterinary Biosciences and Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland and the Folkhälsan Institute of Genetics, Helsinki, Finland – sequence: 6 givenname: Päivi surname: Vanhapelto fullname: Vanhapelto, Päivi organization: Veterinary Clinic Vetset, Kirkkonummi, Finland – sequence: 7 givenname: Hannes surname: Lohi fullname: Lohi, Hannes organization: Department of Veterinary Biosciences and Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland and the Folkhälsan Institute of Genetics, Helsinki, Finland – sequence: 8 givenname: András M surname: Komáromy fullname: Komáromy, András M organization: Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America; Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25198798$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1371_journal_pone_0138943 crossref_primary_10_1371_journal_pone_0114552 crossref_primary_10_1007_s00335_015_9607_6 crossref_primary_10_1017_S0022149X19000889 crossref_primary_10_1111_vop_12448 crossref_primary_10_1111_vop_13079 crossref_primary_10_1242_dmm_027037 crossref_primary_10_1111_age_13118 crossref_primary_10_1371_journal_pone_0183021 |
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ContentType | Journal Article |
Copyright | 2014 Cooper et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 Cooper et al 2014 Cooper et al |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: AEC SA HL AMK. Performed the experiments: AEC SA JSR EHS PV HL AMK. Analyzed the data: AEC SA AD PV HL AMK. Contributed to the writing of the manuscript: AEC SA HL AMK. |
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SubjectTerms | Age Animal models Animals Atrophy Biology and Life Sciences Blindness Continents Discoloration Disease Progression Dog Diseases - pathology Dog Diseases - physiopathology Dogs Electroretinography Epithelium Female Genotypes Heredity Macular degeneration Male Medicine and Health Sciences Mutation Pedigree Phenotype Phenotypes Retina Retinal degeneration Retinal Diseases - pathology Retinal Diseases - physiopathology Retinal Diseases - veterinary Retinal pigment epithelium Retinitis Retinitis pigmentosa Sweden Veterinary colleges Vision |
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Title | A novel form of progressive retinal atrophy in Swedish vallhund dogs |
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