GEO DataSets

(Submitter supplied) Among the fundamental unresolved questions in psychiatry is why symptoms of psychosis, such as auditory hallucinations in schizophrenia, fail to appear until early adulthood. Here we report that in mouse models of 22q11.2 deletion syndrome (22q11DS), a leading genetic cause of schizophrenia, synaptic transmission at thalamocortical inputs to the auditory cortex becomes disrupted later in life, thereby recapitulating the adult onset of psychosis. more...

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL17912

56 Samples

Download data: TXT

(Submitter supplied) Progressive ventricular enlargement is one of the most reproducible and recognizable structural abnormalities in schizophrenia, and is associated with more severe symptoms and poorer clinical outcome. The mechanisms of ventricular enlargement in schizophrenia is unknown. We identified that progressive ventricular enlargement is associated with deceleration of motile cilia beating in ependymal cells lining ventricular walls in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). more...

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL21265

16 Samples

Download data: TXT

(Submitter supplied) 22q11.2 Deletion Syndrome (22q11DS) represents one of the most common known genetic risk factors for the development of psychotic illness, and is also associated with high rates of autistic spectrum disorders (ASD) in childhood. We performed integrated genomic analyses of 22q11DS to identify genes and pathways related to specific phenotypes. Eighty percent of 22q11DS individuals (n=37) carried the typical 3 Mb deletion, with significant variability in the deletion characteristics in the remainder of the sample (n=9). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL6947 GPL10558

112 Samples

Download data: CSV

(Submitter supplied) This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS3478 GDS3479

Platform:

GPL1261

40 Samples

Download data: CEL, EXP

Analysis of hippocampi of Df(16)A/+ animals. Df(16)A/+ animals carry microdeletions of about 1.3Mb in the locus syntenic to human 22q11.2. Individuals with 22q11.2 microdeletions show behavioral and cognitive deficits and are at high risk of developing schizophrenia.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 strain sets

Platform:

GPL1261

Series:

GSE10784

20 Samples

Download data: CEL, EXP

Analysis of prefrontal cortex of Df(16)A/+ animals. Df(16)A/+ animals carry microdeletions of about 1.3Mb in the locus syntenic to human 22q11.2. Individuals with 22q11.2 microdeletions show behavioral and cognitive deficits and are at high risk of developing schizophrenia.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 strain sets

Platform:

GPL1261

Series:

GSE10784

20 Samples

Download data: CEL, EXP

(Submitter supplied) Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex and hippocampus areas between mutant and wild type animals at two early developmental stages (embryonic day 17 and postnatal day 6). These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11180

127 Samples

Download data: CEL

(Submitter supplied) 22q11.2 deletion syndrome (22q11DS) is a common cause of developmental neuropsychiatric disorders, including psychosis, autism and epilepsy. This highly penetrant genetic syndrome provides a unique opportunity to mitigate the challenges raised by the heterogeneity of complex mental disorders and to identify specific neuronal phenotypes. Here, we generated induced pluripotent stem cells from subjects carrying a 3 Mb deletion at the 22q11.2 locus and from controls and differentiated these cells in vitro into three-dimensional organoid resembling the developing cerebral cortex. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

4 Samples

Download data: MTX, TSV

(Submitter supplied) We derived iPSC from individuals carrying a 22q11.2 deletion and controls and differentiated them into 3D cortical organoids.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

175 Samples

Download data: CSV