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Quantitative, waking EEG research on depression.

Abstract

Research published in the past decade that used quantitative indices to evaluate the waking EEG characteristics of depressed patients is reviewed. Methodological problems that make results of different research laboratories difficult to compare include diagnostic heterogeneity of depressed groups, lack of inclusion of control subjects, and differences in the EEG techniques. Despite interpretive problems that arise from such substantial variation, consistencies nevertheless emerge. Unmedicated, actively depressed patients appear to exhibit elevated EEG alpha and beta compared to control subjects. Delta and theta distinguished depressed patients from controls in some single studies, but variation in age, specific diagnostic depression categories, and EEG acquisition and analysis techniques rendered these results less definitive. Quantitative EEG differences that may distinguish depressed subject samples from those with other psychiatric disorders are considered. Factors that limit comparability of the findings are discussed in conjunction with strategies that deserve systematic study in future research.

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BibTeXRIS

V E Pollock, L S Schneider. 1990-04-01. Quantitative, waking EEG research on depression.. https://doi.org/10.1016/0006-3223(90)90591-o

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Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

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Prenatal diagnosis of malformations of cortical development by dedicated neurosonography.

OBJECTIVE: Malformations of cortical development (MCD) are rarely diagnosed in utero. We describe and compare the ultrasonographic and pathology findings in a cohort of fetuses with MCD. METHODS: Fetuses with MCD were identified among all fetuses evaluated for suspected brain anomalies at the Fetal Neurology Clinic, and the ultrasonographic findings were compared with the results of the pathology examination. RESULTS: We suspected the presence of MCD by ultrasonography in 23 fetuses. The mean gestational age at the time of ultrasound diagnosis was 26.2 (range, 18-40) weeks. The ultrasonographic findings leading to the diagnosis of MCD were abnormally overdeveloped gyri and sulci for gestational age (n = 7), delay in sulcation (n = 5), abnormally thin cortex (n = 5) abnormally wide and broad sulci (n = 3), bulging into the lateral ventricle (n = 1), cortical cleft (n = 1), and multiple intraparenchymal echogenic nodules (n = 1). All fetuses had associated central nervous system (CNS) and/or non-CNS anomalies. Pathology examination (performed in 17 fetuses) confirmed MCD in 16. CONCLUSIONS: Cortical malformations can be diagnosed in utero by ultrasonography based on the presence of specific deviations from the normal pattern of development. The identified cases may represent the more severe forms in the MCD spectrum. The pathology findings do not always conform to the current classification systems of MCD but help in differentiating between possible genetic and acquired etiologies and in some cases provide a definitive syndromic diagnosis.

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