Abstract

BackgroundOlfactory dysfunction has repeatedly been observed in individuals diagnosed with schizophrenia. The most stable and consistent finding on the behavioral level is that of smell identification deficits. However, the nature of olfactory identification abnormalities seems to extend to structural abnormalities in the underlying neurobiology of the olfactory system. Furthermore, smell identification deficits are also documented in first-episode patients and non-psychotic first-degree relatives of schizophrenia patients. Family members of schizophrenia patients also show structural abnormalities of the olfactory system, suggesting that these may serve as an endophenotype for the development of schizophrenia.Only a few studies examined the olfactory identification ability in adolescents at-risk for schizophrenia and suggested smell identification deficits as a risk marker for schizophrenia. These studies included adolescents at clinical as well as at genetic risk for schizophrenia. None of these studies focused on children at genetic risk for schizophrenia. Therefore, we investigated the olfactory identification ability in children of parents with schizophrenia in comparison to children of parents without a psychotic disorder. As we are also interested in the specificity of the olfactory impairments to schizophrenia, we included children of parents with bipolar disorder. We hypothesize that children at genetic risk for schizophrenia would have the most severe smell identification deficits and that children of bipolar disorder patients would have less severe deficits than the at-risk for schizophrenia group but more severe than the group of children without a psychotic parent.MethodsParticipants - The olfactory identification ability was assessed in 202 children of schizophrenia patients (‘children at familial risk for schizophrenia’) in relation to that of 200 children of parents without a psychotic disorder (‘controls’). In addition, we also assessed the B-SIT in 120 children of bipolar disorder patients (‘children at familial risk for bipolar disorder’). All children were 7 years of age at the time of assessment and they were part of the Danish High Risk and Resilience Study – VIA7.Brief Smell Identification Test - The Brief Smell Identification Test (B-SIT) contains 12 items that need to be scratched and sniffed. The test has excellent reliability (> 0.80) and demonstrates agreement for abnormal olfaction comparing B-SIT with the San Diego Odor Identification Test (SDOIT). A maximum score of 12 reflects intact olfactory identification functioning. B-SIT has been conducted in patients with neurodegenerative disorders (Parkinson’s disease and Alzheimer’s disease) and can be used for individuals above 5 years of age.Statistics - We will use analysis of covariance (ANCOVA) for analysis of the B-SIT total scores with ‘diagnosis of parent’ as the independent variable and age and sex as covariates for the three groups.ResultsAnalyses will be performed within the next 3 months so can be presented in April 2018.DiscussionConclusion and discussion cannot be drawn at this time.

Highlights

  • Previous studies clearly demonstrated that Minor physical anomalies (MPAs) are significantly increased in schizophrenia

  • The Danish High Risk and Resilience Study – VIA 7 is a prospective cohort study of 522 7-year old children, 202 of them born to at least one parent diagnosed with schizophrenia in the Danish registries, 120 of them born to a least one parent diagnosed with bipolar disorder and 200 of them born to parents without any of these diagnoses

  • We propose that ErbB4 signaling participates in sensorimotor gating dysfunction in schizophrenia by getting involved in somatosensory cortex deficits and GABAergic dysfunction

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Summary

Methods

We assessed the total expression and subcellular localization of proteins involved in ER export processing of GPI-APs from the DLPFC of 15 matched pairs of SCZ and comparison subjects. Discussion: Decreased PGAP1 in an ER enriched fraction in consistent with reduced inositol deacylation and potential dysfunction as the gatekeeper of GPI-AP ER exit in SCZ. This suggests that the GPI-anchor is not correctly modified. We observed unchanged total level of GPI-APs in Triton X-114 phase separation, but a significant decrease in the amount of NCAM and GPC1 that was sensitive to PI-PLC in SCZ. This finding may be consistent with abnormal GPI modification of these two candidate proteins. Ozge Akgul*,1, Emre Bora, Berna Binnur Akdede, Köksal Alptekin1 1Dokuz Eylul University; 2Dokuz Eylül University School of Medicine

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