Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Gut Microbiota in APP/PS1 Transgenic Mouse Model of Alzheimer's Disease

PROVIDER: PRJNA1015445 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26037420_1.fastq.gz	Fastqsanger.gz
	SRR26037420_2.fastq.gz	Fastqsanger.gz
	SRR26037421_1.fastq.gz	Fastqsanger.gz
	SRR26037421_2.fastq.gz	Fastqsanger.gz
	SRR26037422_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 112

Similar Datasets

Transcriptome changes in forebrain neuron-specific farneyltransferase knockout in APP/PS1 mice

Project description:Our study aimed to investigate the biological impact of forebrain neuron-specific farnesyltransferase knockout in a transgenic APP/PS1 Alzheimer's disease model.

2021-08-02 | GSE174314 | GEO

Age-dependent changes in the sarkosyl-insoluble proteome of the APPswe/PS1de9 mouse model of Alzheimer's disease implicate dysfunctional mitochondria in disease pathogenesis

Project description:This study was designed to identify and quantify pre-fibrillary proteins enriched by their insolubility in the detergent sarkosyl. Sarkosyl insoluble fractions were isolated from the brain of APP/PS1 transgenic mouse model of Alzheimer's disease and littermate wild type mice to identify protein aggregates involved in disease pathogenesis.

2020-05-22 | PXD009069 | Pride

APP/PS1 Mouse Brain Effects of ADAM17

Project description:Affects of ADAM17 AAV9 mediated injection on cognitive and vascular function in the APP/PS1 mouse model of Alzheimer's disease.

2023-03-02 | PXD040026 | Pride

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

Partial inhibition of mitochondrial complex I attenuates neurodegeneration and restores energy homeostasis and synaptic function in a symptomatic Alzheimer’s mouse model

Project description:We performed next-generation RNA sequencing (RNA-seq) using brain tissue from 23 months old non-transgenic (NTG), non-treated and CP2 (mitochondrial complex I inhibitor)-treated APP/PS1 (mouse model of Alzheimer`s disease). By comparing transcriptomic data of NTG and vehicle-treated APP/PS1 mice, we found processes affected by the disease in APP/PS1 such as impaired ATP metabolism, ion transport, nervous system development, synaptic transmission, and inflammation. CP2-treatment in APP/PS1 positively affected genes related to immune system, axonogenesis, dendritic spine morphology, synaptic function, among the others. These data demonstrate that pathways improved by CP2 treatment in APP/PS1 mice comprise major pathways essential for therapeutic efficacy in Alzheimer`s disease.

2020-10-31 | GSE149248 | 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

Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer's mouse model and stimulates synaptic plasticity pathway enzymes

Project description:The Ketogenic Diet (KD) improves memory and longevity in aged C57BL/6 mice. We tested 7 months KD vs. control diet (CD) in the mouse Alzheimer's Disease (AD) model APP/PS1. KD significantly rescued Long-Term-Potentiation (LTP) to wild-type levels, not by changing Amyloid-β (Aβ) levels. KD's 'main actor' is thought to be Beta-Hydroxy-butyrate (BHB) whose levels rose significantly in KD vs. CD mice, and BHB itself significantly rescued LTP in APP/PS1 hippocampi. KD's 6 most significant pathways induced in brains by RNAseq all related to Synaptic Plasticity. KD induced significant increases in synaptic plasticity enzymes p-ERK and p-CREB in both sexes, and of brain-derived neurotrophic factor (BDNF) in APP/PS1 females. We suggest KD rescues LTP through BHB's enhancement of synaptic plasticity. LTP falls in Mild-Cognitive Impairment (MCI) of human AD. KD and BHB, because they are an approved diet and supplement respectively, may be most therapeutically and translationally relevant to the MCI phase of Alzheimer's Disease.

2023-12-31 | GSE230469 | GEO

Project description:Exosomal MicroRNAs modulates the cognitive function in Fasudil treated APP/PS1 Transgenic Mouse model of Alzheimer's disease

| PRJNA859243 | ENA

AD and FTLD model mouse, brain, Phosphoproteome

Project description:Using a high-end mass spectrometry, we screened phosphoproteins and phosphopeptides in five types of Alzheimer's disease (AD) mouse models (5xFAD, APP-tg, PS1-tg, PS2-tg and APP-KI) and four types of frontotemporal lobar degeneration (FTLD) mouse models(CHMP2B-KI, PGRN-KI, VCP-KI and TDP43-KI) at multiple time points (1, 3 and 6 months).

2021-09-07 | PXD027119 | Pride

Expression profiling of ncRNAs with custom microarray in 3, 10 and 20 month old wild type and 3xTG AD mice

Project description:In this study, we particularly focused on short ncRNA expression profiling of three, ten and twenty month old triple transgenic mouse model for Alzheimers disease (Oddo et al.; 2003;Neuron). These mice harbor presenilin PS1(M146V), APP(Swedish) and tau(P301L) mutations and develop beta-amyloid plaques and at later stages also a tau pathology. Controls are age matched B6129SF2/J mice.

2014-10-31 | E-MTAB-2738 | 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