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P301S Mutant Tau-Driven Zebrafish Platform Enables Systematic Identification of Pharmacological GSK3β Inhibitors with Anti-Neurodegenerative Efficacy

ABSTRACT: P301S Mutant Tau-Driven Zebrafish Platform Enables Systematic Identification of Pharmacological GSK3β Inhibitors with Anti-Neurodegenerative Efficacy

PROVIDER: PRJNA1248471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33052294_1.fastq.gz	Fastqsanger.gz
	SRR33052294_2.fastq.gz	Fastqsanger.gz
	SRR33052295_1.fastq.gz	Fastqsanger.gz
	SRR33052295_2.fastq.gz	Fastqsanger.gz
	SRR33052296_1.fastq.gz	Fastqsanger.gz

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P301S Mutant Tau-Driven Zebrafish Platform Enables Systematic Identification of Pharmacological GSK3β Inhibitors with Anti-Neurodegenerative Efficacy

Project description:Spatial transcriptome sequencing technology has provided high-resolution transcriptome data for studying the molecular mechanism of Tau P301S mediating Alzheimer's disease-like pathological changes in zebrafish, providing a unique insight into the pathogenesis of tau pathology-mediated cell-cell interactions in AD.

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Abundance of tRNA fragments in Tau-RNA complexes from Tau-mutant PS19 (human P301S Tau transgenic) mice hippocampus

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Project description:Aggregation of the microtubule-associated protein, tau, can lead to neurofibrillary tangle formation in neurons and glia, the hallmark of tauopathy. The cellular damages induced by the tau overexpression and aggregation may lead to multiple pathologic features of tauopathy. However, the effect of aging on tauopathy has not been elucidated yet. Here, we conducted lncRNA/mRNA sequencing analysis on P301S mutant Tau transgenic mouse model (PS19) with different ages to track the genetic changes occurred by the aging and progression of tau overexpression.

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Cdk5i peptide treatment in aged Tau P301S mice

Project description:Cdk5i peptide treatment in aged Tau P301S mice

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Project description:To assess the potential neuroprotective effects of overexpressing skeletal muscle Transcription Factor EB (TFEB) signaling in the context of age-associated neurodegenerative disease pathologies, we derived cTFEB;HSACre transgenic mice in the MAPT P301S tau hyperphosphorylated background and used the Nanostring nCounter® Alzheimer’s Disease panel to gain more precise insights into disease-relevant transcriptional changes in the hippocampus in both male and female mice with both Tau hyperphosphorylation and skeletal muscle TFEB overexpression. We confirmed significantly reduced transcriptional activation of the nCounter AD microglial activation module through signature scoring.

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