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  Abstracts: Eye tracking dysfunction as phenotypic marker in linkage studies with schizophrenia  
  September 06, 1995



R. Lencer(1), V. Arolt(1), S. Purmann(2), A. Nolte(1), B. Müller(3), M. Schürmann(2) and E. Schwinger(2)
(1) Klinik für Psychiatrie und (2) Institut für Humangenetik, Medizinische Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck; (3) Bernhard-Nocht-Institut für Tropenmedizin, Bernhard-Nocht-Str. 74, 20359 Hamburg, Germany  

2nd Workshop Neurogenetics in Germany, Munich, October 19-21, 1995

Eye tracking dysfunction (ETD) has been discussed as a phenotypic marker of genetic liability to schizophrenia. We present results of 9 German families (79 members) with multiple occurrence of schizophrenia. Family members were investigated with regard to: a) psychiatric disorders based on DSM III-R; b) ETD, defined by velocity criteria and the number of saccades occurring during smooth pursuit of a horizontally moving target (30 o/s); c) 12 markers in a candidate region for schizophrenia on chromosome 6p11-p23. ETD resp. schizophrenia was treated as an autosomal dominant trait with penetrances for heterozygotes = 0.8 resp. 0.2 and homozygotes = 0.9 resp. 0.235, gene frequency = 0.01 and probability of affection for non-gene carriers = 0.026 resp. 0.0063. The maximum LOD-score we obtained for ETD by two point analysis is 2.03, = 0.0, at marker D6S426. For disorders of the schizophrenia spectrum the LOD-score is only 1.16, =0.0, at marker D6S274. There is no significant indication of heterogeneity.

In linkage studies in candidate regions for schizophrenia, ETD seems to be a better phenotypic marker than psychopathological symptoms.
Suggestion for a candidate region on chromosome 6p11-p23 is given as proposed by several authors (Kendler et al., Virgina; Wang et al., Bethesda; Wildenauer et al., Munich; Moises et al., Kiel), recently.

Eye tracking dysfunction (ETD)

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