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Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE244010 | GEO | 2024/12/01

REPOSITORIES: GEO

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Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [miRNA-Seq]

Project description:Adults and children with the 22q11.2 deletion syndrome (22q11.2DS) demonstrate cognitive, social and emotional impairments and markedly increased risk for schizophrenia (SCZ). The alterations in early human brain development resulting from this deletion remain unclear. Here we use organoid models of the developing human cerebral cortex derived from patients with 22q11.2DS and SCZ as well as unaffected controls to identify cell-type-specific developmental abnormalities that result from this genomic lesion. Using RNA-sequencing and follow-up experimental validation we find that loss of genes within the 22q11.2 locus leads to delayed development of cortical neurons.

2024-12-01 | GSE244007 | GEO

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [scRNA-Seq]

2024-12-01 | GSE244005 | GEO

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [bulk RNA-Seq]

2024-12-01 | GSE244006 | GEO

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia.

Project description:Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia.

| PRJNA1020883 | ENA

Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome.

Project description:There is increased risk of developing psychosis in 22q11.2 deletion syndrome (22q11DS). Although this condition is associated with morphologic brain abnormalities, simultaneous examination of multiple high-resolution measures of cortical structure has not been performed.Fifty-three patients with 22q11DS, 30 with psychotic symptoms, were compared with demographically matched nondeleted youths: 53 typically developing and 53 with psychotic symptoms. High-resolution magnetic resonance imaging measures of cerebral volume, cortical thickness, surface area, and an index of local gyrification were obtained and compared between groups.Patients with 22q11DS demonstrated global increases in cortical thickness associated with reductions in surface area, reduced index of local gyrification, and lower cerebral volumes relative to typically developing controls. Findings were principally in the frontal lobe, superior parietal lobes, and in the paramedian cerebral cortex. Focally decreased thickness was seen in the superior temporal gyrus and posterior cingulate cortex in 22q11DS relative to nondeleted groups. Patterns between nondeleted participants with psychotic symptoms and 22q11DS were similar but with important differences in several regions implicated in schizophrenia. Post hoc analysis suggested that like the 22q11DS group, cortical thickness in nondeleted individuals with psychotic symptoms differed from typically developing controls in the superior frontal gyrus and superior temporal gyrus, regions previously linked to schizophrenia.Simultaneous examination of multiple measures of cerebral architecture demonstrates that differences in 22q11DS localize to regions of the frontal, superior parietal, superior temporal, and paramidline cerebral cortex. The overlapping patterns between nondeleted participants with psychotic symptoms and 22q11DS suggest partially shared neuroanatomic substrates.

| S-EPMC4446247 | biostudies-literature

22q11.2 deletion syndrome human cortical organoids

Project description:We derived iPSC from individuals carrying a 22q11.2 deletion and controls and differentiated them into 3D cortical organoids.

2020-07-08 | GSE142041 | GEO

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [miRNA-Seq]

Project description:Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [miRNA-Seq]

| PRJNA1020872 | ENA

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [scRNA-Seq]

Project description:Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [scRNA-Seq]

| PRJNA1020881 | ENA

Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [bulk RNA-Seq]

Project description:Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome and schizophrenia. [bulk RNA-Seq]

| PRJNA1020871 | ENA

Schizophrenia and 22q11.2 deletion syndrome.

Project description:22q11.2 deletion syndrome (22qDS) is a genetic syndrome associated with a chromosome 22q11.2 deletion and variable phenotypic expression that commonly includes schizophrenia. Approximately 1% of patients with schizophrenia have 22qDS. The schizophrenia in 22qDS appears broadly similar to that found in the general population with respect to core signs and symptoms, treatment response, neurocognitive profile, and MRI brain anomalies. However, individuals with a 22qDS form of schizophrenia typically have distinguishable physical features, have a lower IQ, and may differ in auxiliary clinical features. IQ, length of 22q11.2 deletions, and COMT functional allele do not appear to be major risk factors for schizophrenia in 22qDS. Ascertainment biases and small sample sizes are limitations of most studies. Larger studies over the lifespan and continuing education about this underrecognized condition are needed. 22qDS-schizophrenia is an important genetic subtype and a valuable model of neurodevelopmental mechanisms involved in the pathogenesis of schizophrenia.

| S-EPMC3129332 | biostudies-other

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