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ABSTRACT: APP/PS1 mice

PROVIDER: PRJEB33984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3478721.fastq.gz	Fastqsanger.gz
	ERR3478722.fastq.gz	Fastqsanger.gz
	ERR3478727.fastq.gz	Fastqsanger.gz
	ERR3478728.fastq.gz	Fastqsanger.gz
	ERR3478729.fastq.gz	Fastqsanger.gz

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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.

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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

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Single-cell sequencing of FACS-sorted mouse astrocytes, investigating the effect of absence of microglia in a mouse model of ß-amyloidopathy

Project description:The APPSwe/PS1dE9 (APP/PS1) mouse ß-amyloidopathy mouse model exhibits extracellular Aß deposition, particularly in the neocortex and hippocampus, increasing steadily from about 6 months, with reactive astrogliosis and synapse loss occurring proximal to plaques. We crossed APP/PS1 mice onto genetically modified mice which lack microglia (Csf1r ∆FIRE/∆FIRE) to assess whether Aß plaque deposition and downstream events are altered in brains lacking microglia.

2024-10-15 | E-MTAB-14233 | biostudies-arrayexpress

RNA-seq of mouse brain tissue investigating the effect of absence of microglia in a mouse model of ß-amyloidopathy

Project description:The APPSwe/PS1dE9 (APP/PS1) ß-amyloidopathy mouse model exhibits extracellular Aß deposition increasing steadily from about 6 months, particularly in the neocortex and hippocampus, with reactive astrogliosis and synapse loss occurring proximal to plaques. We crossed APP/PS1 mice onto genetically modified mice which lack microglia (Csf1r ∆FIRE/∆FIRE) to assess whether Aß plaque deposition and downstream events are altered in brains lacking microglia.

2024-10-15 | E-MTAB-14231 | biostudies-arrayexpress

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (ATAC-Seq)

Project description:The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was used to investigate the AD-associated chromatin reshaping in the APPswe/PS1dE9 (APP/PS1) mouse model. ATAC-seq data in the hippocampus of 8-month-old APP/PS1 mice were generated, and the relationship between chromatin accessibility and gene expression was analyzed in combination with RNA-sequencing.We identified 1690 increased AD-associated chromatin accessible regions in the hippocampal tissues of APP/PS1 mice and 1003 decreased chromatin accessible regions were considered to be related with declined AD-associated biological processes.In the APP/PS1 hippocampus, 1090 genes were found to be up-regulated and 1081 down-regulated. Interestingly, enhanced ATAC-seq signal was found in approximately 740 genes, with 43 exhibiting up-regulated mRNA levels.Our study reveals that alterations in chromatin accessibility may be an initial mechanism in AD pathogenesis.

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Project description:We have previously demonstrated that Sirt3 gene deletion, a model for metabolic syndrome, leads to brain mitochondrial dysfunction and neuroinflammation. We also reported that silencing of Sirt3 gene in APP/PS1 mice results in exacerbation of insulin resistance, neuroinflammation and β amyloid plaque deposition. To further understand how metabolic syndrome and amyloid pathology interact, we performed RNA-seq analysis of the brain samples from wild type, Sirt3-/- , APP/PS1 and APP/PS1/Sirt3-/- mice.

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Total RNA Sequencing in microglia isolated from N-AS treated APP/PS1 mice

Project description:To examine the regulation of microglia by N-AS-triggered SPMs, we analyzed the gene expression patterns of microglia derived from WT, APP/PS1, and N-AS-injected APP/PS1 mice using RNAseq. These results indicated that N-AS-triggered SPMs activated an anti-inflammatory, positive immune response, and enhanced the phagocytic abilities of microglia in N-AS-treated APP/PS1 mice, leading to resolution of neuroinflammation and upregulation of phagocytic microglia in this AD animal model.

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CircTulp4 functions in Alzheimer’s disease pathogenesis by regulating its parental gene Tulp4

Project description:Here, we systematically investigated circRNAs in the APP/PS1 model mouse brain through deep RNA-sequencing. We report that circRNAs are markedly enriched in the brain and that several circRNAs exhibit differential expression between wild-type and APP/PS1 mice. We characterized one abundant circRNA, circTulp4, derived from Intron1 of the gene Tulp4. To investigate the effect of CircTulp4 on chromatin status, we used ATAC-seq to investigate the chromatin accessibility upon CircTulp4 knockdown.

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Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (RNA-Seq)

2020-07-09 | GSE145907 | GEO

Moxibustion Improves Hypothalamus Aqp4 Polarization in APP/PS1 Mice: Evidence from Spatial Transcriptomics

Project description:Aquaporin-4 (AQP4) is highly polarized to perivascular astrocytic endfeet. Loss of AQP4 polarization is associated with many diseases. In Alzheimer's disease (AD), it is found that AQP4 loos its normal location and thus reduce the clearance of amyloid-β plaques and Tau protein. Clinical and experimental studies show that moxibustion can improve the learning and memory abilities of AD. In order to explore whether moxibustion can affect the polarization of AQP4 around blood brain barrier (BBB), we used spatial transcriptomics (ST) to analyze the expression and polarization of Aqp4 in wild type mice, APP/PS1 mice and APP/PS1 mice intervened by moxibustion. The results showed that moxibustion improved the loss of abnormal polarization of AQP4 in APP/PS1 mice, especially in the hypothalamic BBB. Besides, there are other 31 genes with Aqp4 as the core have the similar depolarization in APP/PS1 mice, most of which are also membrane proteins. The majority of them have been reversed by moxibustion. At the same time, we employed the cerebrospinal fluid circulation gene set, which was found being on a higher level in the group of APP/PS1 mice with moxibustion treatment. Finally, in order to further explore its mechanism, we analyzed the mitochondrial respiratory chain complex enzymes closely related to energy metabolism, and found that moxibustion can significantly increase the expression of mitochondrial respiratory chain enzymes such as Cox6a2 in the hypothalamus, which could provide energy for mRNA transport. Our research shows that increasing the polarization of hypothalamic Aqp4 through mitochondrial energy supply may be an important target for moxibustion to improve APP/PS1 mice’s cognitive impairment.

2023-02-22 | GSE222981 | GEO

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