Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355399 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression of PS19 Tau Transgenic mice from hippocampus at different ages 3, 6, 9, and 12 months We used Affy arrays to understand the global expression profile of PS19 Tau transgenic mice
2018-08-28 | GSE89979 | GEO
Project description:We report the binding between tRNA fragments and Phosphorylated Tau pS396 from the hippocampus of WT controls and Tau-mutant PS19 (human P301S Tau transgenic) mice. We show tRNA fragments abundance in Tau-RNA complexes changes between the two groups. Specific tRNA fragment in the results of Real Time-qPCR were consistent with the small RNA microarray:5'tRF_GluCTC
2025-05-14 | GSE297027 | GEO
Project description:A role for the type I transmembrane trafficking receptor SORLA in reducing Aβ levels has been well-established, however, virtually nothing is known with respect to whether and how SORLA can potentially affect tau pathology. Here, we show that transgenic SORLA upregulation (SORLA TG) can reverse pathological effects in aged PS19 (P301S tau) mouse brain, including tau phosphorylation, ventricle dilation, synapse loss, LTP impairment and glial hyperactivation. Proteomic analysis indicates reversion of PS19 profiles in PS19/SORLA TG hippocampus, including pathological changes in synapse-related proteins as well as key drivers of synaptic dysfunction such as Apoe and C1q. snRNAseq analysis reveals suppression of PS19-dependent signatures with SORLA upregulation, including proinflammatory induction of Plxnb1/Plxnb2 in glial cell types. PlxnB1/B2 expression as well as other neuroinflammatory features are exacerbated in PS19 hippocampus with SORLA deletion. Together, these results implicate a global role for SORLA in neuroprotection from tau toxicity in PS19 mouse brain.
2026-05-24 | PXD056276 | Pride
Project description:A role for the type I transmembrane trafficking receptor SORLA in reducing Aβ levels has been well-established, however, virtually nothing is known with respect to whether and how SORLA can potentially affect tau pathology. Here, we show that transgenic SORLA upregulation (SORLA TG) can reverse pathological effects in aged PS19 (P301S tau) mouse brain, including tau phosphorylation, ventricle dilation, synapse loss, LTP impairment and glial hyperactivation. Proteomic analysis indicates reversion of PS19 profiles in PS19/SORLA TG hippocampus, including pathological changes in synapse-related proteins as well as key drivers of synaptic dysfunction such as Apoe and C1q. snRNAseq analysis reveals suppression of PS19-dependent signatures with SORLA upregulation, including proinflammatory induction of Plxnb1/Plxnb2 in glial cell types. PlxnB1/B2 expression as well as other neuroinflammatory features are exacerbated in PS19 hippocampus with SORLA deletion. Together, these results implicate a global role for SORLA in neuroprotection from tau toxicity in PS19 mouse brain.
2026-05-24 | GSE278215 | GEO
Project description:A role for the type I transmembrane trafficking receptor SORLA in reducing Aβ levels has been well-established, however, virtually nothing is known with respect to whether and how SORLA can potentially affect tau pathology. Here, we show that transgenic SORLA upregulation (SORLA TG) can reverse pathological effects in aged PS19 (P301S tau) mouse brain, including tau phosphorylation, ventricle dilation, synapse loss, LTP impairment and glial hyperactivation. Proteomic analysis indicates reversion of PS19 profiles in PS19/SORLA TG hippocampus, including pathological changes in synapse-related proteins as well as key drivers of synaptic dysfunction such as Apoe and C1q. snRNAseq analysis reveals suppression of PS19-dependent signatures with SORLA upregulation, including proinflammatory induction of Plxnb1/Plxnb2 in glial cell types. PlxnB1/B2 expression as well as other neuroinflammatory features are exacerbated in PS19 hippocampus with SORLA deletion. Together, these results implicate a global role for SORLA in neuroprotection from tau toxicity in PS19 mouse brain.
2026-05-24 | GSE278067 | GEO
Project description:Protein kinase CK2α’ is upregulated in patients with tau-associated dementias and in the PS19 mouse model of tauopathy. CK2α’ haploinsufficiency in the PS19 mouse model improved tau pathology, synaptic density, synaptic function, cognitive behavior and disease-associated microglia phenotypes. We hypothesized CK2α’ haploinsufficiency would impact dysregulated gene expression in the PS19 model. We found that CK2α’ haploinsufficiency led to enhanced synaptic gene network expression and enhance immune gene network expression.
2026-02-06 | GSE298505 | GEO
Project description:By introducing haploinsufficiency of Cx3cr1 in the P301S (PS19) transgenic model of tau pathology, we report remarkable transcriptional changes, including crucial amyotrophic lateral sclerosis and Alzheimer’s disease risk genes, several of which showed co-expression, suggesting gene–gene interactions among these genetic risk factors.
2026-03-09 | GSE305471 | GEO
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
2014-12-04 | GSE61417 | GEO
Project description:Abundance of tRNA fragments in Tau-RNA complexes from Tau-mutant PS19 (human P301S Tau transgenic) mice hippocampus
| PRJNA1262409 | ENA
Project description:Tau aggregates are critical pathological features of Alzheimer’s disease (AD) and other tauopathies. Growing evidence suggests that soluble tau aggregates trigger neurodegenerative phenotypes. However, the nature of the tau species and interactors involved in its aggregation and spreading remains unclear. By using size exclusion chromatography, mass spectrometry, and bioinformatic analysis, we identified Bassoon protein (BSN) as a significant tau interactor in PS19 mice, as well as in human AD and PSP cases. We also found that overexpression of BSN triggers the aggregation of tau and increase the tau seeding activity in vitro, and also exacerbates the degenerative phenotype in a Fly model for tauopathy. Knockdown of BSN significantly reduced tau spreading in PS19 mouse brains and destabilized the tau aggregates, leading to a reduction in the tau pathology in this model. Furthermore, BSN downregulation was able to restore the neurodegenerative phenotype in PS19 mice, observed in electrophysiology and behavioral tests. Our results identify BSN as a key interactor of tau spread and aggregation in the brain, and therefore a potential target for the treatment of diseases that involve tau spread and aggregation.
2023-03-11 | PXD027451 | Pride