Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA expression profiles in WT and APP/PS1 mouse hippocampus

ABSTRACT: With the criterion of 2-fold cutoff, 7 miRNAs were upregulated and 7 miRNAs were downregulated in APP/PS1 hippocampal tissues compared with WT hippocampal tissues

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE53859 | GEO | 2014/01/08

SECONDARY ACCESSION(S): PRJNA233584

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MicroRNA expression profiles in WT and APP/PS1 mouse hippocampus

Project description:With the criterion of 2-fold cutoff, 7 miRNAs were upregulated and 7 miRNAs were downregulated in APP/PS1 hippocampal tissues compared with WT hippocampal tissues Microarray analysis of miRNAs was performed on pooled hippocampal tissues from WT (n=16) and APP/PS1 mice (n=16) at E14

2014-01-08 | E-GEOD-53859 | biostudies-arrayexpress

miRNA profile in the hippocampus of APP/PS1 transgenic mice

Project description:To explore the miRNAs associated with the memory deficits in Alzheimer's disease, we detected the miRNA profiles in the hippocampus of 6-month-old male APPswe/PS1dE9 (APP/PS1) mice and age-matched wild type C57BL/6 mice.

2019-10-04 | GSE138382 | GEO

Expression data from C57/6J mice (Normal), APP/PS1 mice and APP/PS1 mice treatment with HPYD

Project description:Aβ is a peptide of 39-42 amino acid residues that derived from putative intramembranous processing of amyloid precursor protein (APP) at the proposed active site of the γ-secretase/PS1 aspartyl. Aβ has been shown to aggregate and accumulate abnormally in the brain of AD (Alzheimer's disease), and extracellular amyloid plaques of Aβ peptides aggregation can trigger a cascade of pathologic events leading to nerve fiber entanglement and neuronal apoptosis protease. We used microarrays to investigate the effects of HPYD on the gene expression of APP/PS1 transgenic mice, the brain tissues of control group, model group and HPYD group mice.

2018-02-23 | GSE104249 | GEO

APP/PS1 mice characterization and time progression.

Project description:RNA samples from the cerebral cortex of APP/PS1 and WT mouse littermates aged 3, 6 and 12 months were analyzed using the Affymetrix Genechip Mouse Gene 1.1 ST Array. The APP-PS1 transgenic mouse express the human mutated forms APPswe and PS1dE9. This is a good model of familial Alzheimer Disease because it reproduces several features of the disease as β-amyloid deposits throughout the brain and exhibit memory impairment by the end of the sixth month and is a simple model to study the molecular pathways. The aim of this study is to identify dysregulation of inflammation pathways in order to understand shifts of inflammation responses with disease progression.

2014-04-30 | E-MTAB-2121 | biostudies-arrayexpress

Total RNA sequencing in the hippocampus of wild type and APP/PS1 mice

Project description:Our study aimed to dissect differentially expressed circRNAs in the hippocampus of wild type and APP/PS1 mice and demonstrated the important role of circRNA in Alzheimer's disease.

2020-10-05 | GSE158995 | GEO

RNA-seq of hippocampal samples from IL-18KO/APP/PS1 , WT, IL-18KO, and APP/PS1 mice.

Project description:The goal of the experiment was to understand the role of IL-18 in Alzheimers disease. Gene expression was examined in the hippocampus of wild type mice and the APP/PS1 mice (which are a mouse model for Alzheimers disease) that either encoded IL-18 or had the IL-18 gene knocked out.

2017-12-31 | E-MTAB-5668 | biostudies-arrayexpress

Age- and Nicotine-Associated Gene Expression Changes in the Hippocampus of APP/PS1 Mice

Project description:The etiology of Alzheimer's disease (AD) has been intensively studied. However, little is known about the molecular alterations in early-stage and late-stage AD. Hence, we performed RNA sequencing and assessed differentially expressed genes (DEGs) in the hippocampus of 18-month and 7-month-old APP/PS1 mice. Moreover, the DEGs induced by treatment with nicotine, the nicotinic acetylcholine receptor agonist that is known to improve cognition in AD, were also analyzed in old and young APP/PS1 mice. When comparing old APP/PS1 mice with their younger littermates, we found an upregulation in genes associated with calcium overload, immune response, cancer, and synaptic function; the transcripts of 14 calcium ion channel subtypes were significantly increased in aged mice. In contrast, the downregulated genes in aged mice were associated with ribosomal components, mitochondrial respiratory chain complex, and metabolism. Through comparison with DEGs in normal aging from previous reports, we found that changes in calcium channel genes remained one of the prominent features in aged APP/PS1 mice. Nicotine treatment also induced changes in gene expression. Indeed, nicotine augmented glycerolipid metabolism, but inhibited PI3K and MAPK signaling in young mice. In contrast, nicotine affected genes associated with cell senescence and death in old mice. Our study suggests a potential network connection between calcium overload and cellular signaling, in which additional nicotinic activation might not be beneficial in late-stage AD

2019-09-10 | GSE86828 | GEO

Early amyloid-induced changes in microglia gene expression in APP/PS1 mice [scRNA-seq]

Project description:Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia, characterized by deposition of extracellular amyloid-beta (Aβ) aggregates and intraneuronal hyperphosphorylated Tau. Many AD risk genes, identified in genome-wide association studies (GWAS), are expressed in microglia, the innate immune cells of the central nervous system. Specific subtypes of microglia emerged in relation to AD pathology, such as disease-associated microglia (DAMs), which increased in number with age in amyloid mouse models and in human AD cases. However, the initial transcriptional changes in these microglia in response to amyloid are still unknown. Here, to determine early changes in microglia gene expression, hippocampal microglia from APPswe/PS1dE9 (APP/PS1) mice and wildtype littermates were isolated and analyzed by RNA sequencing (RNA-seq). By bulk RNA-seq, transcriptomic changes were detected in hippocampal microglia from 6-months-old APP/PS1 mice. By performing single cell RNA-seq of CD11c-positive and negative microglia from 6-months-old APP/PS1 mice and analysis of the transcriptional trajectory from homeostatic to CD11c-positive microglia, we identified a set of genes that potentally reflect the initial response of microglia to Aβ.

2024-04-01 | GSE226938 | GEO

RNA-seq of hippocampal samples from IL-18KO/APP/PS1 , WT, IL-18KO, and APP/PS1 mice.

Project description:RNA-seq of hippocampal samples from IL-18KO/APP/PS1 , WT, IL-18KO, and APP/PS1 mice.

| PRJEB20583 | ENA

Early amyloid-induced changes in microglia gene expression in APP/PS1 mice [bulk RNA-seq]

2024-04-01 | GSE226937 | GEO