Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NeuID is a novel neuron-specific lncRNA that regulates neuronal function in Alzheimer’s disease [ChIP-seq]

ABSTRACT: Non-coding RNAs are transcripts that do not encode proteins and comprise 98.5% of the human transcriptome. Among these, long non-coding RNAs (lncRNAs) have been implicated in various biological functions, including the control of gene expression and translation. The central nervous system (CNS) harbors a diverse array of lncRNA transcripts, yet the functions of many remain largely unexplored. In this study, we employed FANS with total RNA-sequencing and single-nuclei RNA sequencing approaches using human and mouse brain tissue to identify novel lncRNAs specific to neurons, and potentially associated with neurodegenerative diseases. We discovered a novel brain-specific lncRNA, the we named 'NeuID', that is specifically expressed in neuronal cells in the mouse and human brains. NeuID expression was found to be reduced in the brains of Alzheimer’s disease (AD) patients. Knockdown (KD) of NeuID resulted in the downregulation of synaptic plasticity genes. Additionally, NeuID KD led to decreased dendritic spine density and reduced neuronal network activity in MEA recordings. Furthermore, we demonstrate that NeuID interacts with EZH2, a component of the PRC2 complex, and mediates the h3k27me3 levels of Olig2 transcription factor. Notably, CRISPRa mediated overexpression of NeuID resulted in the rescue of functional impairment caused by AD-related pathological Aβ oligomers. Overall, our findings identify a novel brain and neuron-exclusive lncRNA that regulates neuronal function, is dysregulated in AD, and might be a potential therapeutic target against neuronal pathology in AD.

ORGANISM(S): Mus musculus

PROVIDER: GSE296334 | GEO | 2026/05/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

NeuID is a novel neuron-specific lncRNA that regulates neuronal function in Alzheimer’s disease

Project description:Non-coding RNAs are transcripts that do not encode proteins and comprise 98.5% of the human transcriptome. Among these, long non-coding RNAs (lncRNAs) have been implicated in various biological functions, including the control of gene expression and translation. The central nervous system (CNS) harbors a diverse array of lncRNA transcripts, yet the functions of many remain largely unexplored. In this study, we employed FANS with total RNA-sequencing and single-nuclei RNA sequencing approaches using human and mouse brain tissue to identify novel lncRNAs specific to neurons, and potentially associated with neurodegenerative diseases. We discovered a novel brain-specific lncRNA, the we named 'NeuID', that is specifically expressed in neuronal cells in the mouse and human brains. NeuID expression was found to be reduced in the brains of Alzheimer’s disease (AD) patients. Knockdown (KD) of NeuID resulted in the downregulation of synaptic plasticity genes. Additionally, NeuID KD led to decreased dendritic spine density and reduced neuronal network activity in MEA recordings. Furthermore, we demonstrate that NeuID interacts with EZH2, a component of the PRC2 complex, and mediates the h3k27me3 levels of Olig2 transcription factor. Notably, CRISPRa mediated overexpression of NeuID resulted in the rescue of functional impairment caused by AD-related pathological Aβ oligomers. Overall, our findings identify a novel brain and neuron-exclusive lncRNA that regulates neuronal function, is dysregulated in AD, and might be a potential therapeutic target against neuronal pathology in AD.

2026-04-01 | GSE296012 | GEO

Prdm16os is a brain and astrocyte-specific lncRNA implicated with Alzheimer’s disease

Project description:Astrocytes provide crucial support for neurons, contributing to synaptogenesis, synaptic maintenance, and neurotransmitter recycling. Under pathological conditions, deregulation of astrocytes contributes to neurodegenerative diseases such as Alzheimer’s disease (AD), highlighting the growing interest in targeting astrocyte function to address early phases of AD pathogenesis. While most research in this field has focused on protein-coding genes, non-coding RNAs, particularly long non-coding RNAs (lncRNAs), have emerged as significant regulatory molecules. In this study, we identified the lncRNA PRDM16-DT as highly enriched in the human brain, where it is almost exclusively expressed in astrocytes. PRDM16-DT and its murine homolog, Prdm16os, are downregulated in the brains of AD patients and in AD models. In line with this, knockdown of PRDM16-DT and Prdm16os revealed its critical role in maintaining astrocyte homeostasis and supporting neuronal function by regulating genes essential for glutamate uptake, lactate release, and neuronal spine density through interactions with the RE1-Silencing Transcription factor (Rest) and Polycomb Repressive Complex 2 (PRC2). Notably, CRISPR-mediated overexpression of Prdm16os mitigated functional deficits in astrocytes induced by stimuli linked to AD pathogenesis. These findings underscore the importance of PRDM16-DT in astrocyte function and its potential as a novel therapeutic target for neurodegenerative disorders characterized by astrocyte dysfunction.

2025-01-03 | GSE271196 | GEO

Genome-wide identification and differential expression of long non-coding RNAs in hypoxic zebrafish brain

Project description:Long non-coding RNAs (lncRNAs) are the master regulators of numerous biological processes. Hypoxia causes oxidative stress with severe and detrimental effects on brain function and acts as a critical initiating factor in the pathogenesis of Alzheimer's disease (AD). From the RNA-Seq in the forebrain (Fb), midbrain (Mb), and hindbrain (Hb) regions of hypoxic and normoxic zebrafish, we identified novel lncRNAs, whose potential cis targets showed involvement in neuronal development and differentiation pathways. Under hypoxia, several lncRNAs and mRNAs were differentially expressed. Co-expression studies indicated that the Fb and Hb regions' potential lncRNA target genes were involved in the AD pathogenesis. In contrast, those in Mb (cry1b, per1a, cipca) was responsible for regulating circadian rhythm. We identified specific lncRNAs present in the syntenic regions between zebrafish and humans, possibly functionally conserved. We thus identified several conserved lncRNAs as the probable regulators of AD genes (adrb3b, cav1, stat3, bace2, apoeb, psen1, s100b).

2020-07-14 | GSE153687 | GEO

LncRNA RVRL1 restricts rabies virus infection by disrupting PRC2 complex [ChIP-seq]

Project description:Rabies is an ancient infectious disease but still lacking efficient therapeutic approach despite of vaccine. In this study, we have identified a novel cytoplasmic lncRNA, namely rabies virus related lncRNA 1(RVRL1), whose expression in neuronal cells is up-regulated upon the infection of the causative agent of rabies, the neurotropic virus rabies virus (RABV). RVRL1 effectively inhibits RABV infection both in neuronal cells and in a mouse model. RVRL1 binds to EZH2 and disrupts the PRC2 complex, which is consistent with the inverse relationship between RVRL1 expression and the cellular H3K27me3 level. RVRL1 expression positively regulates the expression of PCP4L1 encoding a 10 kD peptide, which is shown to inhibit RABV replication. These findings highlight a novel mechanism for lncRNAs to upregulate the expression of antiviral genes, and define two potential anti-rabies reagents including an antiviral lncRNA and an antiviral peptide.

2020-09-08 | GSE107285 | GEO

LncRNA RVRL1 restricts rabies virus infection by disrupting PRC2 complex [RNA-seq]

2020-09-08 | GSE107277 | GEO

Transcriptome Sequencing During Mouse Brain Development Identifies Long Non-Coding RNAs Functionally Involved in Neurogenic Commitment

Project description:Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem cell commitment during neurogenesis. M-bM-^@M-^\LncRNAs control neurogenesisM-bM-^@M-^] Aprea, Prenninger, Dori, Monasor, Wessendof, Zocher, Massalini, Ghosh, Alexopoulou, Lesche, Dahl, Groszer, Hiller, Calegari, The EMBO Journal (In Press) mRNA profiles of Proliferating Progenitors, Differentiating Progenitors and Neurons from lateral cortex of E14.5 mouse embryos. Each cell type in three biological replicates.

2013-11-18 | E-GEOD-51606 | biostudies-arrayexpress

LncRNA and circRNA expression profiles of Aβ25-35-induced AD mice hippocampus treated with Tripterygium Glycoside

Project description:Tripterygium glycosides (TG) was reported to have effect of ameliorating Alzheimer's disease (AD). However, the mechanism is not clear. We aimed to investigate the lncRNAs and circRNAs expression profiles of AD treated with TG by using microarray. LncRNAs, mRNA and circRNA in 3 AD mice and 3 AD+TG mice hippocampal were detected by microarray. The most differentially expressed lncRNAs, mRNA and circRNA in AD+TG group were screened. The differentially expressed lncRNAs and circRNAs were analyzed for GO enrichment and KEGG pathway. Co-expression analysis of lncRNAs and mRNA was performed by calculating correlation coefficients. Protein-protein interaction (PPI) network analysis was performed on mRNAs using STRING. LncRNA-target-TFs network were analyzed by Network software. CircRNA-mirNA network were conducted by Cytoscape software. A total of differentially expressed 661 lncRNAs, 64 circRNAs and 503 mRNAs were detected in AD mice treated with TG. The Pou4f1, Egr2, Mag, and Nr4a1 were the hub genes in the PPI network. The KEGG results showed the mRNAs that co-expressed with lncRNAs were enriched in TNF, PI3K-Akt, and Wnt signaling pathway. lncRNA-target-TFs network analysis indicated the TFs including Cebpa, Zic2, and Rxra were the most likely to regulate the detected lncRNAs. The circRNA-miRNA interaction network indicated 275 miRNAs may bind to the 64 circRNAs. In conclusion, the findings supplied a novel perspective for AD pathogenesis. And the detected lncRNAs, mRNAs, and circRNAs might be novel therapeutics targets for AD.

2022-05-30 | GSE204817 | GEO

Molecular Signatures Underlying Selective Regional Vulnerability to Alzheimer's Disease

Project description:Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive impairment and neurodegeneration as a result of abnormal neuronal loss. To elucidate the molecular systems associated with AD, we characterized the gene expression changes associated with multiple clinical and neuropathological traits in 1,053 postmortem brain samples across 19 brain regions from 125 persons dying with varying severities of dementia and variable AD-neuropathology severities. 125 human brains were accessed from the Mount Sinai/JJ Peters VA Medical Center Brain Bank (MSBB). This brain resource was assembled after applying stringent inclusion/exclusion criteria and represents the full spectrum of clinical and neuropathological disease severity in the absence of discernable non-AD neuropathology. RNA samples from 19 brain regions isolated from the 125 MSBB specimens were collected and profiled using Affymetrix Genechip microarrays. There were 50 to 60 subjects per brain region with varying degrees of AD pathological abnormalities.

2016-08-19 | E-GEOD-84422 | biostudies-arrayexpress

The human lncRNA GOMAFU suppresses neuronal interferon response pathways affected in schizophrenia

Project description:Long noncoding RNAs (lncRNAs) play multifaceted roles in regulating molecular networks that underlie normal brain function and the complex etiology of neuropsychiatric disorders. One example is the human neuronal lncRNA GOMAFU, which was reported to display abnormal expression in schizophrenia (SCZ) postmortem brains, regulate alternative splicing of SCZ risk gene transcripts, and harbor genetic variates contributing to the risk of SCZ. However, functional targets and molecular networks regulated by GOMAFU have not been determined. How GOMAFU dysregulation contributes to SCZ pathogenesis remains elusive. Here we report that GOMAFU is a novel modulator of neuronal interferon (IFN) response pathways. We found ectopic changes of GOMAFU in a brain region-specific manner from transcriptomic profiling datasets derived from multiple SCZ cohorts. Using CRISPR-Cas9 to delete the GOMAFU promoter, we identified hundreds of human neuronal GOMAFU targets in various SCZ-affected molecular pathways, with the most striking effects on upregulation of numerous genes enriched in IFN signaling pathways. In addition, GOMAFU targets in the IFN pathways are differentially affected in SCZ postmortem brain regions and negatively associated with GOMAFU abundance. Furthermore, acute exposure to IFN- caused a marked decline of GOMAFU, leading to selective upregulation of a subclass of GOMAFU targets in stress and immune response pathways, which are also affected in SCZ brains and form a highly interactive molecular network. Together, our studies revealed novel roles of GOMAFU in governing the neuronal IFN pathways and suggest that GOMAFU dysregulation may contribute to the etiological neuroinflammatory responses in SCZ brain neurons.

2022-06-24 | GSE206720 | GEO

Transcriptome analyses reveal enrichment of specific lncRNAs in specific brain regions and neuronal populations

Project description:Despite the availability of large-scale transcriptomics data, specific long noncoding RNAs (lncRNAs) expressed in specific brain regions and populations of neurons are poorly understood. Here we report analysis of expression of lncRNAs and mRNAs expressed in hippocampus and prefrontal cortex (PFC), two regions of brain that are involved in memory storage and neuropsychiatric disorders. Our unbiased analyses have identified specific lncRNAs and mRNAs that are enriched in hippocampus and PFC. We have identified several regions in the chromosomes characterized by clustered lncRNA expression suggesting the transcriptional hotspots of lncRNA in the genome. We find that, a subset of lncRNAs and protein coding genes in their vicinity are uniquely co-expressed in specific brain regions and thus presumably co-regulated. Furthermore, specific brain regions and neuronal populations have characteristic lncRNA expression profile. These studies reveal unexpected complexity in the expression profiles of lncRNAs in the mammalian brain.

2015-03-06 | GSE61401 | 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