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Braus, Barbara Katharina (2008): Zum Sudden Acquired Retinal Degeneration Syndrome (SARDS) beim Hund. Dissertation, LMU München: Tierärztliche Fakultät



The subject of the study was to investigate the aetiology of SARDS. Following an initial literature review, patient data and clinical findings from 39 Patients were collected and analysed. One specific observation was that one third of all patients comprised Dachshunds and that 51.3 % of affected animals were female neutered. The average age of SARDS patients was found to be 8.8 years (range 3 months to 13 years). The ophthalmoscopic appearance of the fundus of SARDS patients was documented at different stages of the disease during serial examinations with the help of fundus photography. This revealed degenerative retinal changes which were found to progress linear following the onset of SARDS, finally resembling dogs with severe generalised progressive retinal degeneration. In the second part of the study, the hypothesis that SARD is an autoimmune disease, was tested with the help of autoantibody screening. In a first step, serum from 24 SARDS patients and 14 normal controls were assessed for autoantibodies to the purified autoantigens S-Antigen and CRALBP with the help of a western blot. No difference in the incidence of autoantibodies could be found between SARDS patients and healthy controls while testing the well known autoantigens S-antigen and CRALBP. In a second step, an attempt was made to identify new autoantigens by testing the entire retinal proteom as an autoantigenic source, again using Western blot techniques. Following the initial detection of a reaction against a specific protein found almost exclusively in SARDS patients, it was possible to identify this protein with the help of mass spectrometry (MALDI/TOF/TOF) as NSE. These findings were verified by the binding of IgG antibodies to purified NSE in 25% of the SARDS patients and 0% of the normal control dogs. The results of this study suggest that an autoimmune aetiology of SARDS involving autoantibodies against NSE is possible. However, it is unclear whether these play a causative role in SARDS or whether they are the result of retinal destruction by another mechanism. Further investigations into a possible autoimmune aetiology of SARDS are therefore indicated and the role of NSE as an autoantigen must be further assessed.