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Mus musculus

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

PROVIDER: PRJNA342656 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4238600_1.fastq.gz	Fastqsanger.gz
	SRR4238600_2.fastq.gz	Fastqsanger.gz
	SRR4238601_1.fastq.gz	Fastqsanger.gz
	SRR4238601_2.fastq.gz	Fastqsanger.gz
	SRR4238602_1.fastq.gz	Fastqsanger.gz

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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

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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.

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Project description:In a series of slice electrophysiology experiments, we demonstrated that female APPSwe-Psen1dE9 Alzheimer's disease model mice show greater impairments in hippocampal synaptic plasticity than male mice of the same age and genotype. Female APP/PS1 mice also showed greater impairments in behavioural associative memory, higher amyloid plaque burden and increased microglial activation in the hippocampus than males at age 4-5 months. We thus profiled hippocampal mRNA from these mice to investigate the underlying molecular mechanisms. Compared to wild-type mice of the same sex, we found that female APP/PS1 mice showed a greater upregulation of microglial and inflammatory genes than males. Moreover, downregulation of genes associated with memory and plasticity was observed uniquely in female APP/PS1 mice. These data provide insight into the potential mechanisms of the greater prevalence and faster progression of AD in females.

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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:MicroRNA expression profiles in WT and APP/PS1 mouse hippocampus

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Project description:Synaptic dysfunction occurs early in Alzheimer´s disease. However, efforts to protect against these detriments have not been possible due to the inadequate understanding of synaptic signalling pathways involved in the neuropathological disease process. The aim of this study was to elucidate the molecular mechanisms behind Alzheimer´s and synaptic plasticity-related signalling using a multi-omics and in situ imaging approach. We used an Alzheimer´s mouse model (APPswe/PSN1dE9, age of 12 month) (APP/PS1) and compared the changes on the proteome including global phosphorylation and N-linked glycosylation pattern, pathway-focused transcriptome and neurological disease-associated miRNAome with age-matched control mice in the neocortex, hippocampus, olfactory bulb and brainstem. Our analysis showed that signalling pathways related to synaptic functions associated to dendritic spine morphology, neurite outgrowth, long-term potentiaiton, CREB signalling and cytoskeletal dynamics were altered in the APP/PS1 transgenic mice, particular in the neocortex and olfactory bulb. This was associated with Aβ plaques and neurofibrillary tangle formation as well as microglial clustering in all brain regions except brainstem. The responses may be epigenetically modulated by the interaction with a number of miRNAs. We suggest that the alterations in synaptic plasticity-related signalling are associated to neurocognitive dysfunctions that resemble the situtation in human AD patients.

2016-05-11 | PXD003312 | Pride

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