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Mus musculus

ABSTRACT: microRNA-seq of TPR50 Tau P301S Transgenic Mouse in different brain regions and time-points

PROVIDER: PRJNA354345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5030840.fastq.gz	Fastqsanger.gz
	SRR5030850.fastq.gz	Fastqsanger.gz
	SRR5030860.fastq.gz	Fastqsanger.gz
	SRR5030870.fastq.gz	Fastqsanger.gz
	SRR5030880.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:RNA-seq of TPR50 Tau P301S Transgenic Mouse in different brain regions and time-points

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Transcriptomic analysis of RNA-sequencing data from nontransgenic and transgenic tau SPAM mice

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S-nitrosylation in P301S mouse tauopathy model

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2019-11-08 | PXD010106 | Pride

LncRNA/mRNA sequencing analysis on cerebral cortex of P301S mutant Tau transgenic mice (PS19).

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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RNA-seq and TRAP-seq of astrocytes and brain tissue in mouse models of Alzheimer's pathology

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2021-12-02 | E-MTAB-10985 | biostudies-arrayexpress

Humanized APOE genotypes influence lifespan independently of tau aggregation in the P301S mouse model of tauopathy

Project description:To gain insight into the role of human APOE on tau-associated neurodegeneration, we examined P301S mutant tau transgenic mice carrying humanized APOE alleles

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CNS cell-type specific gene profiling of aging P301S tau transgenic mice

Project description:RNA sequencing of cortex from young (3mo) and old (10mo) P301S tau transgenic mice

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SnRNA-seq analysis of hippocampus in TAFE3 and TAFE4 mice

Project description:The apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer disease (AD). In addition to effects of apoE on amyloid-β, results have shown that apoE markedly influences pathological forms of tau and tau-mediated neurodegeneration with apoE4 having a strong deleterious effect on both parameters. In the brain, apoE is produced and secreted primarily from astrocytes and also by activated microglia though the cell-specific role of each form of apoE in the setting of neurodegeneration has not been determined. We utilized a well- characterized mouse model of tauopathy, P301S Tau transgenic mice expressing floxed APOE-e4 or APOE-e3 alleles. We crossed these mice with Aldh1l1-CreERT2 mice and at 5.5 months of age, after the onset of tau pathology, administered tamoxifen or vehicle. We then compared mice with or without inducible knockout of astrocyte APOE at 9.5 months of age. Single nucleus RNA sequencing analysis revealed striking gene expression changes in all cell types in P301S mice with astrocytic APOE4 playing a role in modulating neuron, astrocyte, and microglial gene expression to a more homeostatic state.

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Chronic intermittent hypoxia enhances pathological tau seeding, propagation, and accumulation, and exacerbates Alzheimer’s-like memory and synaptic plasticity deficits and molecular signatures

Project description:Obstructive sleep apnea (OSA), characterized by sleep fragmentation and chronic intermittenthypoxia (CIH), is a risk factor for Alzheimer’s disease (AD) progression. Recent epidemiologicalstudies point to CIH as the best predictor of developing cognitive decline and AD in elderly withOSA. However, the precise underlying mechanism(s) remain unknown. The present study wasundertaken to evaluate the effect of CIH on pathological human tau seeding, propagation, andaccumulation, cognition, synaptic plasticity, neuronal network excitability, and gene expressionprofiles in a P301S human mutant tau mouse model of AD and related tauopathies. We exposed 4-4.5-month-old, male, P301S and WT mice to an 8-week CIH protocol (6 min cycle:21% O 2 to 8% O 2 to 21% O 2 , 80 cycles per 8 h during daytime), and assessed its effect on taupathology and various AD-related phenotypic and molecular signatures. Age- and gender-matched P301S and WT mice were reared in normoxia (21% O 2 ) as experimental controls. CIH significantly enhanced pathological human tau seeding and spread across connected brain circuitry in P301S mice; it also increased phospho-tau load. CIH also exacerbated memory and synaptic plasticity deficits in P301S mice. However, CIH had no effect on seizure susceptibility and network hyperexcitability in these mice. Finally, CIH exacerbated AD-related pathogenic molecular signaling in P301S mice. CIH-induced increase in pathologic human tau seeding and spread and exacerbation of other AD- related impairments provide new insights into the role of CIH and OSA in AD pathogenesis.

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H3K9ac data from mouse models suggest structural changes in the murine brain epigenome that involve the nuclear lamina

Project description:To explore whether tau-related epigenomic changes that we found human brain H3K9ac data (Synapse ID: syn4896408) are recapitulated in mouse models known to accumulate tau, we generated hippocampal H3K9ac ChIP-seq profiles from two different mouse models each at an early and a late stage of neurodegeneration. Specifically, we studied 6 and 11 months old mutant tau mice (MAPT P301S), which start to accumulate phosphorylated tau in neurons by 6 months. Wild-type mice of the same age were used as controls. The second mouse model was the CK-p25 model, which is characterized by increased amyloid-β levels early after p25 induction followed by increased tau phosphorylation and neuronal loss at later stages. Three months old CK-p25 mice were studied 2 weeks and 6 weeks after p25 induction and compared with CK littermate controls.

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