Sensory Deficits in Schizophrenia and Psychosis
Deficits in the expression of cortical oscillations in schizophrenia suggest that the neural networks generating these oscillations are not functioning optimally. Spencer et al.
(pages 369–375) report that the power and phase-locking of the 40 Hz auditory steady-state oscillatory response is reduced in first-episode patients diagnosed with schizophrenia and affective disorder (mainly bipolar).
Deficits in auditory sensory gating are related to the inability to filter out irrelevant input. Brockhaus-Dumke et al.
(pages 376–384) present evidence that deficits in auditory sensory gating are present in patients at risk for schizophrenia prior to the onset of the full-blown psychosis, as well as in patients in their first episode of schizophrenia prior to the onset of antipsychotic treatment. Thus, the sensory gating deficits appear to be an early sign of schizophrenia and are not a consequence of antipsychotic treatment.
Deficits in the cortical electrical response to changes in auditory input, mismatch-negativity (MMN), may be a heritable feature of schizophrenia. However, Magno et al.
(pages 385–391) report that MMN was normal in first-degree healthy biological relatives and in first-episode schizophrenia patients. This finding questions the relationship between MMN deficits and the heritable risk for schizophrenia.
Quednow et al.
(pages 434–437) provide evidence that two related variations (polymorphisms) in the gene coding for the serotonin-2A (5-HT2A
) receptor are related to the extent of prepulse inhibition of the startle response, a form of sensory gating, in a group of 68 patients diagnosed with schizophrenia.
Psychosis: Genetic Risk and Association Studies
There is quite strong evidence that the Neuregulin 1 (NRG1
) gene plays a role in susceptibility to schizophrenia. Georgieva et al.
(pages 419–427) analyzed a large family based genetic association sample of 876 trios with these disorders and found evidence that NRG1
is a susceptibility gene for bipolar disorder as well as schizophrenia. These data also suggest that different risk variants might differentially be associated with aspects of the psychosis phenotype.
Hall et al.
(pages 428–433) show that genetic variation in the D-amino acid oxidase activator (DAOA
) gene, which has been associated with schizophrenia, results in alterations in brain function in individuals at risk of the disorder. In particular, risk-associated variants of the gene resulted in decreased activation of the hippocampus, a brain region implicated in psychosis.
Soronen et al.
(pages 438–442) report on their association study of the most promising candidate genes for psychotic disorders (DAOA
) and bipolar disorder. The data did not reveal any strong evidence for association of the studied genes with bipolar or psychotic disorder. Instead, the nonsynonymous DAOA variant associated strongly with visuospatial ability.
© 2008 Published by Elsevier Inc. All rights reserved.