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

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

PROVIDER: PRJEB42003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4992200_1.fastq.gz	Fastqsanger.gz
	ERR4992200_2.fastq.gz	Fastqsanger.gz
	ERR4992201_1.fastq.gz	Fastqsanger.gz
	ERR4992201_2.fastq.gz	Fastqsanger.gz
	ERR4992202_1.fastq.gz	Fastqsanger.gz

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RETRACTED: circTulp4 functions in Alzheimer’s disease pathogenesis by regulating its parental gene, Tulp4

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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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Peripherally-expressed apoE4 impairs brain functions and exacerbates amyloid pathogenesis by compromising cerebrovascular functions

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Project description:Neuroinflammation and activation of innate immunity are pathological hallmarks of Alzheimer’s disease (AD). In contrast, very few studies have examined the impact of the adaptive immune system in AD pathogenesis. In this study, we find that genetic deletion of peripheral immune populations significantly accelerates amyloid pathogenesis, worsens neuroinflammation, and alters microglial activation state. We used microarray analysis to profile gene expression underlying genotype related changes at the cellular level in the context of AD .

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Peripherally-expressed apoE4 impairs brain functions and exacerbates amyloid pathogenesis by compromising cerebrovascular functions

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GSAP regulates mitochondrial function through Mitochondria-associated ER membrane in the pathogenesis of Alzheimer’s disease

Project description:Gamma-secretase activating protein (GSAP) plays an important role in regulating gamma-secretase activity and specificity, which contributes to the pathogenesis of Alzheimer’s disease (AD) and Down syndrome. GSAP is expressed in a variety of cell types in the bain. To elucidate the molecular function of GSAP across different cell types in the brain, we performed single nuclei RNA sequencing (sn-RNAseq) on hippocampal tissues obtained from wildtype (WT) and GSAP knockout (GKO) mice. To further investigate the pathogenic function of GSAP in the AD progression, we also determined effects of GSAP gene deletion in the J20 AD mouse model through sn-RNAseq on hippocampal tissues obtained from J20;WT and J20;GKO mice.

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A systems-biology approach connects aging mechanisms with Alzheimer’s disease pathogenesis [TCPY]

Project description:A systems-biology approach connects aging mechanisms with Alzheimer’s disease pathogenesis [TCPY]

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