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Superior temporal gyrus spectral abnormalities in schizophrenia.

ABSTRACT: Considerable evidence indicates early auditory stimulus processing abnormalities in schizophrenia, but the mechanisms are unclear. The present study examined oscillatory phenomena during a paired-click paradigm in the superior temporal gyrus (STG) as a possible core problem. The primary question addressed is whether first click and/or second click group differences in the time-domain evoked response in patients with schizophrenia are due to (1) group differences in the magnitude of poststimulus oscillatory activity, (2) group differences in poststimulus phase-locking, and/or (3) group differences in the magnitude of ongoing background oscillatory activity. Dense-array magnetoencephalography from 45 controls and 45 patients with schizophrenia produced left- and right-hemisphere STG 50- and 100-ms time-frequency evoked, phase-locking, and total power measures. Whereas first click 100-ms evoked theta and alpha abnormalities were observed bilaterally, evoked low beta-band differences were specific to the left hemisphere. Compared to controls, patients with schizophrenia showed more low-frequency phase variability, and the decreased 100-ms S1 evoked response observed in patients was best predicted by the STG phase-locking measure.

SUBMITTER: Edgar JC

PROVIDER: S-EPMC2685182 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature

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Superior temporal gyrus spectral abnormalities in schizophrenia.

Edgar J Christopher JC Hanlon Faith M FM Huang Ming-Xiong MX Weisend Michael P MP Thoma Robert J RJ Carpenter Bruce B Hoechstetter Karsten K Cañive José M JM Miller Gregory A GA

Psychophysiology 20080724 5

Considerable evidence indicates early auditory stimulus processing abnormalities in schizophrenia, but the mechanisms are unclear. The present study examined oscillatory phenomena during a paired-click paradigm in the superior temporal gyrus (STG) as a possible core problem. The primary question addressed is whether first click and/or second click group differences in the time-domain evoked response in patients with schizophrenia are due to (1) group differences in the magnitude of poststimulus ...[more]

PMID: 18665866

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Project description:Glycosylation is a post-translational modification that is an essential element in cell signaling and neurodevelopmental pathway regulation. Glycan attachment can influence the tertiary structure and molecular interactions of glycosylated substrates, adding an additional layer of regulatory complexity to functional mechanisms underlying central cell biological processes. One type of enzyme-mediated glycan attachment, fucosylation, can mediate glycoprotein and glycolipid cell surface expression, trafficking, secretion, and quality control to modulate a variety of inter- and intracellular signaling cascades. Building on prior reports of glycosylation abnormalities and evidence of dysregulated glycosylation enzyme expression in schizophrenia, we examined the protein expression of 5 key fucose-modifying enzymes: GDP-fucose:protein O-fucosyltransferase 1 (POFUT1), GDP-fucose:protein O-fucosyltransferase 2 (POFUT2), fucosyltransferase 8 (FUT8), fucosyltransferase 11 (FUT11), and plasma ?-l-fucosidase (FUCA2) in postmortem superior temporal gyrus of schizophrenia (N=16) and comparison (N=14) subjects. We also used the fucose binding protein, Aleuria aurantia lectin (AAL), to assess ?-1,6-fucosylated N-glycoprotein abundance in the same subjects. In schizophrenia, we found increased expression of POFUT2, a fucosyltransferase uniquely responsible for O-fucosylation of thrombospondin-like repeat domains that is involved in a non-canonical endoplasmic reticulum quality control pathway. We also found decreased expression of FUT8 in schizophrenia. Given that FUT8 is the only ?-1,6-fucosyltransferase expressed in mammals, the concurrent decrease in AAL binding in schizophrenia, particularly evident for N-glycoproteins in the ~52-58kDa and ~60-70kDa molecular mass ranges, likely reflects a consequence of abnormal FUT8 expression in the disorder. Dysregulated FUT8 and POFUT2 expression could potentially explain a variety of molecular abnormalities in schizophrenia.

Project description:ObjectiveIndividuals with 22q11.2 deletion syndrome are known to be at high risk of developing schizophrenia. Previous imaging studies have provided limited data on the relation of schizophrenia expression in 22q11.2 deletion syndrome to specific regional brain volumetric changes. The authors hypothesized that the main structural brain finding associated with schizophrenia expression in 22q11.2 deletion syndrome, as for schizophrenia in the general population, would be gray matter volumetric deficits, especially in the temporal lobes.MethodMR brain images from 29 patients with 22q11.2 deletion syndrome and schizophrenia and 34 comparison subjects with 22q11.2 deletion syndrome and no history of psychosis were analyzed using a voxel-based morphometry method that also yielded volumes for related region-of-interest analyses. The authors compared data from the two groups using an analysis of covariance model correcting for total intracranial volume, age, sex, IQ, and history of congenital cardiac defects. The false discovery rate threshold was set at 0.05 to account for multiple comparisons.ResultsVoxel-based morphometry analyses identified significant gray matter reductions in the left superior temporal gyrus (Brodmann's area 22) in the schizophrenia group. There were no significant between-group differences in white matter or CSF volumes. Region-of-interest analyses showed significant bilateral gray matter volume reductions in the temporal lobes and superior temporal gyri in the schizophrenia group.ConclusionsThe structural brain expression of schizophrenia associated with the highly penetrant 22q11.2 deletion involves lower gray matter volumes in temporal lobe regions. These structural MRI findings in a 22q11.2 deletion syndrome form of schizophrenia are consistent with those from studies involving schizophrenia samples from the general population. The results provide further support for 22q11.2 deletion syndrome as a genetic subtype and as a useful neurodevelopmental model of schizophrenia.

Dataset Information

Superior temporal gyrus spectral abnormalities in schizophrenia.

Publications

Superior temporal gyrus spectral abnormalities in schizophrenia.

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