Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from the neuron model of Alzheimer's disease (AD)

ABSTRACT: To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment. One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells compared with wild-type cells. Comparative analyses of PS1P117L cells and wild-type cells showed that the expression of genes involved in cellular assembly and organization, cellular function and maintenance, and tissue development were significantly altered.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80244 | GEO | 2016/12/01

SECONDARY ACCESSION(S): PRJNA318424

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein

Project description:To delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment. One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells with rhTFAM treatment compared with those without the treatment. Comparative analyses of PS1P117L cells with or without rhTFAM treatment showed that the expression of genes involved in protein synthesis, gene expression, and cancer were significantly altered. From these microarray analyses, we found that the expression levels of the genes associated with neuritogenesis were decreased in PS1P117L neurons compared with those in the wild type, and that hTFAM significantly increased these gene expression.

2016-12-01 | GSE80245 | GEO

Expression data from Alzheimer's disease (AD) model mouse and AD model mouse overexpressing human mitochondrial transcriptional factor A (hTFAM)

Project description:To delineate the mechanism underlying the amelioration of AD pathophysiology by hTFAM, we performed gene expression profiling using hippocampal RNAs from the AD model mouse and AD model mouse overexpressing human TFAM. One-way ANOVA of microarray data from hippocampus revealed that the gene expression profile is most significantly altered in the hippocampi of ADh/hTFAMh mice. Comparative analyses of the brains of ADh/WT and ADh/hTFAMh mice showed that the expression of genes involved in cancer, endocrine system disorders, and organismal injury and abnormalities were significantly altered. Among the genes whose expression was significantly altered by hTFAM expression, transthyretin, encoded by the Ttr gene, binds Aβ and inhibits its aggregation.

2016-12-01 | GSE80242 | GEO

Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points

Project description:Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease and the most common form of dementia. AD is characterized by progressive memory loss and cognitive decline, affecting behavior, speech, and motor abilities. The neuropathology of AD includes the formation of extracellular amyloid-β plaques and intracellular neurofibrillary tangles of phosphorylated tau, as well as neuronal loss. Although neuronal loss is a primary hallmark of AD, non-neuronal cell populations are known to maintain brain homeostasis and neuronal health through neuron-glia and glial cell crosstalk via chemical messengers. To investigate altered glia-neuron communication in the presence of amyloid-β and tau pathology, we generated snRNA-seq data from the hippocampus of 3xTg-AD mice at 6 and 12 months and age-matched wild-type littermates. We predicted altered glia-neuron interactions between senders (astrocytes, microglia, oligodendrocytes, and OPCs) and receivers (excitatory and inhibitory neurons) across time points. We further investigated these interactions through pseudo-bulk differential expression, functional enrichment, and gene regulatory analyses.

2025-02-24 | GSE261596 | GEO

Sequencing of ponatinib-resistant LC-2/ad derivatives (PR1 and PR2) and parental LC-2/ad cells

Project description:Sequencing of ponatinib-resistant LC-2/ad derivatives (PR1 and PR2) and parental LC-2/ad cells was performed in order to determine mechanisms of acquired resistance in the PR1 and PR2 cell lines. NRAS p.Q61K mutation identified in PR1 cells. Upregulation of wild-type EGFR signaling identified in PR2 cells.

2017-04-21 | GSE98030 | GEO

The role of aD in sepsis

Project description:aD is one of the b2 integrin family members. The role of aD in sepsis has not been examined yet. aD is previously reported to be expressed on neutrophils. We performed cecal ligation and puncture sepsis model in wild type and aD knockout and examined the role of aD in neutrophils.

2022-10-17 | GSE215749 | GEO

Expression data from Alzheimer's disease model mouse

2013-04-17 | GSE36981 | GEO

Expression data from Alzheimer's disease model mouse

Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and AlzheimerM-bM-^@M-^Ys disease. 3xTg-AD-H mice harboring a homozygous Psen1M146V mutation and homozygous mutant transgenes for APPSwe and tauP301L, 3xTg-AD-h mice harboring hemizygous APPSwe and tauP301L transgenes with a homozygous Psen1M146V mutation, and non-transgenic control mice (non-Tg) were used in this study, (male, n=3 for each group). RNA samples prepared from hippocampi were subjected to microarray analysis using the Affymetrix Mouse Gene 1.0 ST platform (GPL6246).

2013-04-17 | E-GEOD-36981 | biostudies-arrayexpress

Expression data from post mortem Alzheimer's disease brains

2013-04-17 | GSE36980 | GEO

bacTRAP profiling of seven different types of neurons , vulnerable and resistant to Alzheimer's disease (AD) across the lifetime of the mouse

Project description:We report here the bacTRAP (bacterial artificial chromosome , translating ribosome affinity purification) profiling of 7 different types of neurons in the mouse, at three different ages: two neuron types very vulnerable to AD (principal cells of entorhinal cortex layer II - ECII), pyramidal cells of hippocampus CA1, and 5 types of neurons more resistant to AD (pyramidal cells of hippocampus CA2 and CA3, granule neurons of the dentate gyrus, pyramidal cells from layer IV of primary visual cortex V1, and pyramidal cells from layer II/III and V of primary somatosensory cortex S1). Using these profiles we generated molecular signatures for each of these cell types, proved that the molecular identity of these cell types is very well conserved across mouse and humans, and constructed functional networks for each cell type that allowed us to identify genes and pathways associated with selective neuronal vulnerability in AD. We also report the profiling of ECII neurons in APP/PS1 mice (a mouse model of Abeta accumulation) at 6 months of age.

2020-05-30 | GSE151460 | GEO

Expression data from post mortem Alzheimer's disease brains

Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease. We prepared RNA samples from the gray matter of frontal and temporal cortices and hippocampi derived from 88 postmortem brains, among which 26 cases were pathologically diagnosed as having AD or an AD-like disorder. High-quality RNA (RIN≧6.9) samples were subjected to microarray analysis using the Affymetrix Human Gene 1.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 1.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 33 frontal cortex samples, among which 15 were from AD patients; 29 temporal cortex samples, among which 10 were from AD patients; 17 hippocampus samples, among which seven were from AD patients

2013-04-17 | E-GEOD-36980 | biostudies-arrayexpress

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