BACKGROUND: Disruption of arachidonic acid pathways and prostaglandin signalling has been implicated in the pathophysiology of schizophrenia. AIMS: We intended to study prostaglandin signalling in groups of young schizophrenia patients, first-degree relatives, and healthy controls in order to assess effects of heritability on this biological marker-one important endophenotype criterion. METHOD: Namely, we assessed intensity of methylnicotinate skin flushing using optical reflection spectroscopy. Tests were applied to 19 adolescent first-episode schizophrenia patients, 21 first-degree relatives, and groups of age and gender matched healthy controls. RESULTS: Compared to healthy controls, attenuation of skin flushing at low niacin concentrations was found only in schizophrenia patients, but not in first-degree relatives. CONCLUSION: While our results indicate niacin hyposensitivity as reliable biological marker in schizophrenia, they do not provide clear evidence for its heritability. Particularly, the results in adolescent schizophrenia patients are suggestive for the perception of attenuated niacin flushing as secondary to the pathophysiology at the onset of schizophrenic illness, namely increased oxidative stress, alterations of unspecific immune-response or inflammation-like processes.
BACKGROUND: Disruption of arachidonic acid pathways and prostaglandin signalling has been implicated in the pathophysiology of schizophrenia. AIMS: We intended to study prostaglandin signalling in groups of young schizophreniapatients, first-degree relatives, and healthy controls in order to assess effects of heritability on this biological marker-one important endophenotype criterion. METHOD: Namely, we assessed intensity of methylnicotinate skin flushing using optical reflection spectroscopy. Tests were applied to 19 adolescent first-episode schizophreniapatients, 21 first-degree relatives, and groups of age and gender matched healthy controls. RESULTS: Compared to healthy controls, attenuation of skin flushing at low niacin concentrations was found only in schizophreniapatients, but not in first-degree relatives. CONCLUSION: While our results indicate niacin hyposensitivity as reliable biological marker in schizophrenia, they do not provide clear evidence for its heritability. Particularly, the results in adolescent schizophreniapatients are suggestive for the perception of attenuated niacinflushing as secondary to the pathophysiology at the onset of schizophrenic illness, namely increased oxidative stress, alterations of unspecific immune-response or inflammation-like processes.
Authors: Michael S McCloskey; Antonia S New; Larry J Siever; Marianne Goodman; Harold W Koenigsberg; Janine D Flory; Emil F Coccaro Journal: J Psychiatr Res Date: 2009-02-18 Impact factor: 4.791
Authors: Stefan Smesny; Christian E H Schmelzer; Anke Hinder; Alexandra Köhler; Christiane Schneider; Maria Rudzok; Ulrike Schmidt; Berko Milleit; Christine Milleit; Igor Nenadic; Heinrich Sauer; Reinhard H H Neubert; Joachim W Fluhr Journal: Schizophr Bull Date: 2012-05-15 Impact factor: 9.306
Authors: Jeffrey K Yao; George G Dougherty; Clara H Gautier; Gretchen L Haas; Ruth Condray; John W Kasckow; Benjamin L Kisslinger; John A Gurklis; Erik Messamore Journal: Schizophr Bull Date: 2015-09-14 Impact factor: 9.306
Authors: Gregor E Berger; Stefan Smesny; Miriam R Schäfer; Berko Milleit; Kerstin Langbein; Uta-Christina Hipler; Christine Milleit; Claudia M Klier; Monika Schlögelhofer; Magdalena Holub; Ingrid Holzer; Michael Berk; Patrick D McGorry; Heinrich Sauer; G Paul Amminger Journal: PLoS One Date: 2016-02-19 Impact factor: 3.240