Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PROTEOMIC SIGNATURE OF THE CEREBELLUM IN SCHIZOPHRENIA

ABSTRACT: Malfunction of multiple regions in distributed brain circuits has been suggested to underlie the diversity of symptoms and cognitive impairments in schizophrenia. The cerebellum, as part of this circuit, may contribute to these symptoms for this reason we undertook a proteomic profile of this region. Here, we design a quantitative exploratory proteomic analysis in pooled grey matter of the cerebellum from schizophrenia and control individuals with the aim of discovering consistently altered biomarker proteins in schizophrenia.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain

DISEASE(S): Schizophrenia

SUBMITTER: Ricard Rodriguez-Mias

LAB HEAD: Judit Villen

PROVIDER: PXD008216 | Pride | 2020-06-22

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	18820_Percolator_set_Uniprot_Searches.fasta	Fasta
	18820_Percolator_set_Uniprot_Searches.pep.xml	Pepxml
	p02025.raw	Raw
	p02026.raw	Raw
	p02027.raw	Raw

Items per page:

1 - 5 of 22

Similar Datasets

Analysis Of Molecular Networks In The Cerebellum In Chronic Schizophrenia: Modulation By Early Postnatal Life Stressors In Murine Models

Project description:Despite the growing importance of the cortico-cerebellar-thalamo-cortical circuit in schizophrenia, limited information is available regarding altered molecular networks in cerebellum. To identify altered protein networks, we conducted proteomic analysis of grey matter of postmortem cerebellar cortex in chronic schizophrenia subjects (n=12) and healthy individuals (n=14) followed by an extensive bioinformatic analysis. Two double-hit postnatal stress murine models for SZ were used to validate the most robust candidates.

2021-12-30 | PXD024937 | Pride

Transcription profiling of human cerebellum from schizophrenia patients and normal subjects

Project description:Analysis of cortical samples corresponding to the crus I/VIIa area of the cerebellum from schizophrenia patients. A study indicates that targets of the RNA-binding ELAV-like protein HuD are overexpressed in the prefrontal cortex of patients with schizophrenia.

2007-06-22 | E-GEOD-4036 | biostudies-arrayexpress

ANALYSIS OF NETWORKS IN THE DORSOLATERAL PREFRONTAL CORTEX IN CHRONIC SCHIZOPHRENIA: RELEVANCE OF ALTERED IMMUNE RESPONSE

Project description:The dorsolateral prefrontal cortex (DLPFC) is the association area in the anterior part of the frontal lobe and has a crucial role in cognitive functioning and negative symptoms in SZschizophrenia. However, limited information of altered protein networks is available in this region in schizophrenia. We performed a proteomic analysis using single-shot liquid chromatography-tandem mass spectrometry of grey matter of postmortem DLPFC in chronic schizophrenia subjects (n=20) and healthy individuals (n=20) followed by bioinformatic analysis to identify altered protein networks in SZ.

2023-05-10 | PXD024939 | Pride

Schizophrenia-associated methylomic variation: molecular signatures of disease and polygenic risk burden across multiple brain regions (cerebellum DBCBB).

Project description:Genetic association studies provide evidence for a substantial polygenic component to schizophrenia, although the neurobiological mechanisms underlying the disorder remain largely undefined. Building on recent studies supporting a role for developmentally regulated epigenetic variation in the molecular etiology of schizophrenia, this study aimed to identify epigenetic variation associated with both a diagnosis of schizophrenia and elevated polygenic risk burden for the disease across multiple brain regions. Genome-wide DNA methylation was quantified in 262 post-mortem brain samples, representing tissue from four brain regions (prefrontal cortex, striatum, hippocampus and cerebellum) from 41 schizophrenia patients and 47 controls. We identified multiple disease-associated and polygenic risk score-associated differentially methylated positions and regions, many residing in the vicinity of genes previously implicated in schizophrenia including NCAM1, SYNPO, GBP4, PRDM9, GADD45B and DISC1. Our study represents the first analysis of epigenetic variation associated with schizophrenia across multiple brain regions and highlights the utility of polygenic risk scores for identifying molecular pathways associated with etiological variation in complex disease.

2016-11-10 | GSE89702 | GEO

Cerebellum Alzheimer's Disease

Project description:Ion channel splice array data from cerebellum brain tissue samples collected from Alzheimer's disease patients. Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

2010-06-11 | E-GEOD-6777 | biostudies-arrayexpress

Transcriptome of Ts1Cje and euploids cerebellum

Project description:Transcriptome analysis of Ts1Cje (mouse model of Down syndrome) and euploids murine cerebellum during postnatal development Keywords = Down syndrome Keywords = Chromosome 21 Keywords = Transcriptome Keywords = Microarray Keywords = Cerebellum Keywords = Development Keywords: other

2004-12-05 | GSE1611 | GEO

Expression data from the human cerebellum brain

Project description:Schizophrenia (SCZ) and bipolar disorder (BD) are highly heritable psychiatric disorders. Associated genetic and gene expression changes have been identified, but many have not been replicated and have unknown functions. We identified groups of genes whose expressions varied together, that is co-expression modules, then tested them for association with SCZ. Using weighted gene co-expression network analysis, we show that two modules were differentially expressed in patients versus controls. One, upregulated in cerebral cortex, was enriched with neuron differentiation and neuron development genes, as well as disease genome-wide association study genetic signals; the second, altered in cerebral cortex and cerebellum, was enriched with genes involved in neuron protection functions. The findings were preserved in five expression data sets, including sets from three brain regions, from a different microarray platform, and from BD patients. From those observations, we propose neuron differentiation and development pathways may be involved in etiologies of both SCZ and BD, and neuron protection function participates in pathological process of the diseases.

2012-12-31 | GSE35974 | GEO

Pro‐inflammatory activation of microglia in the cerebellum hyperexcites Purkinje cells to trigger ataxia

Project description:Specific medications to combat cerebellar ataxias, a group of debilitating movement disorders characterized by difficulty with walking, balance and coordination. Notably, cerebellar microglial activation appears to be a common feature in different types of ataxic patients and rodent models. However, the causal link between the activation of microglia in the cerebellum and ataxias remains inconclusive. In the present study, using a classic mouse model of cerebellar ataxia induced by 3-acetylpyridine (3-AP), we find a early-onset and long-lasting microglial activation accompanied by neuronal loss and dysfunction in the cerebellum. Transcriptome and behavior analyses indicate that microglial depletion in 3-AP ataxic mice decreases neuroinflammatory response in the cerebellum and rescues the ataxic motor symptoms including motor incoordination, gait abnormality, and locomotor dysfunction. Moreover, specific chemogenetic activation of cerebellar microglia in the vermis by M3D(Gq), a designer receptor exclusively activated by designer drugs (DREADDs), directly induces an expression of pro-inflammatory cytokines and aggravates ataxic motor deficits of 3-AP mice. On the contrary, inhibition of cerebellar microglial activation by M4D(Gi) or minocycline reduces the production of pro-inflammatory cytokines including TNF-α and alleviates motor deficits. Furthermore, blockage of TNF-α signaling attenuates the microglial-triggered hyperactivity of Purkinje cells (PCs). These results suggest that cerebellar microglial activation aggravates neuroinflammatory response, and subsequently induces dysfunction of PCs, which in turn triggers ataxic motor deficits. Our findings thus reveal a causal relationship between pro-inflammatory activation of cerebellar microglia and the ataxic motor symptoms, which may offer novel evidence for therapeutic intervention for cerebellar ataxias by targeting microglia and microglia-derived inflammatory mediators.

2023-07-01 | GSE221991 | GEO

Cerebellum Alzheimer's Disease

Project description:Ion channel splice array data from cerebellum brain tissue samples collected from Alzheimer's disease patients. Keywords: disease associated splicing changes

2007-01-23 | GSE6777 | GEO

ILS/ISS Cerebellum Comparison Affy430

Project description:Inbred Long-Sleep (ILS) and Inbred Short-Sleep (ISS) mice exhibit a large difference in a number of alcohol and drug related behaviors. This study examined the expression levels of transcripts in these strains in the cerebellum, which is a major target of ethanol’s actions in the CNS, in order to find differentially expressed candidate genes for these phenotypes. Cerebellum was specifically chosen due to the fact that Purkinje cell sensitivity to ethanol in these strains is highly correlated to "sleep time", the measure of ethanol sensitivity used with these strains. Naive mice were used because differences in sensitivity are observed upon initial exposure to ethanol. Keywords: cerebellum, naive, untreated

2005-12-02 | GSE3071 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data