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ABSTRACT: RNA-seq for ad/ab LCM in lettuce

PROVIDER: PRJNA780374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16961919_1.fastq.gz	Fastqsanger.gz
	SRR16961919_2.fastq.gz	Fastqsanger.gz
	SRR16961920_1.fastq.gz	Fastqsanger.gz
	SRR16961920_2.fastq.gz	Fastqsanger.gz
	SRR16961921_1.fastq.gz	Fastqsanger.gz

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Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [short RNA]

Project description:To detect miRNAs in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)

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microRNA-132/212 deficiency enhances Ab production and senile plaque deposition in Alzheimerâs disease triple transgenic mice

Project description:The abnormal regulation of amyloid-b (Ab) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimerâs disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Ab deposition and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Ab metabolism, including Tau, Mapk, and Sirt1. We used RNA-Seq to analyse the hippocampus of 3xTg-AD mice lacking the miR-132/212 cluster as well as Neuro2a cells overexpressing miR-132 mimics.

2016-07-17 | E-GEOD-84481 | biostudies-arrayexpress

microRNA-132/212 deficiency enhances Ab production and senile plaque deposition in Alzheimer’s disease triple transgenic mice

Project description:The abnormal regulation of amyloid-b (Ab) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimer’s disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Ab deposition and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Ab metabolism, including Tau, Mapk, and Sirt1.

2016-07-17 | GSE84481 | GEO

Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [lncRNA]

Project description:To detect total RNA in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)

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Project description:INTRODUCTION: Omics studies have revealed that various brain cell types undergo profound molecular changes in Alzheimer’s disease (AD) but the spatial relationships with plaques and tangles and APOE-linked differences remain unclear. METHODS: We performed laser capture microdissection of Ab plaques, the 50mm halo around them, tangles with the 50mm halo around them, and areas distant (>50mm) from plaques and tangles in the temporal cortex of AD and control donors, followed by RNA-sequencing. RESULTS: Ab plaques exhibited upregulated microglial (neuroinflammation) and downregulated neuronal (neurotransmission/energy metabolism) genes, whereas tangles had mostly downregulated neuronal genes. Ab plaques had more differentially expressed genes than tangles. We identified a gradient Ab plaque>peri-plaque>tangle>distant for these changes. AD APOEe4 homozygotes had greater changes than APOEe3 across locations, especially within Ab plaques. DISCUSSION: Transcriptomic changes in AD consist primarily of neuroinflammation and neuronal dysfunction, are spatially associated mainly with Ab plaques, and are exacerbated by the APOEe4 allele.

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