MRNA array in brain tissue samples of 5XFAD mice
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ABSTRACT:
PROVIDER: PRJNA834111 | ENA |
REPOSITORIES: ENA
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Project description:In Alzheimer's disease pathology, several neuronal processes are dysregulated by excitotoxicity including neuroinflammation and oxidative stress (OS). New therapeutic agents capable of modulating such processes are needed to foster neuroprotection. Here, the effect of an optimised NMDA receptor antagonist, UB-ALT-EV and memantine, as a gold standard, have been evaluated in 5XFAD mice. Following treatment with UB-ALT-EV, nor memantine, changes in the calcineurin (CaN)/NFAT pathway were detected. UB-ALT-EV increased neurotropic factors (Bdnf, Vgf and Ngf) gene expression. Treatments reduced astrocytic and microglial activation as revealed by GFAP and Iba-1 quantification. Interestingly, only UB-ALT-EV was able to reduce gene expression of Trem2, a marker of microglial activation and NF-κB. Pro-inflammatory M1-microglial phenotype (Il-1β, Ifn-γ, Ccl2 and Ccl3) markers were down-regulated in UB-ALT-EV-treated mice but not in memantine-treated mice. Interestingly, the anti-inflammatory markers of the M2-migroglial phenotype, chitinase-like 3 (Ym1) and Arginase-1 (Arg1), were up-regulated after treatment with UB-ALT-EV. Since iNOS gene expression decreased after UB-ALT-EV treatment, a qPCR array containing 84 OS-related genes was performed. We found changes in Il-19, Il-22, Gpx6, Ncf1, Aox1 and Vim gene expression after UB-ALT-EV. In sum, our results reveal a robust effect on neuroinflammation and OS processes after UB-ALT-EV treatment, surpassing the memantine effect in 5XFAD.
2023-05-02 | GSE202061 | GEO
Project description:Transcriptome analysis of hippocampal RNA samples from wild-type, 5xFAD, 5xFAD;eIF2α+/S51A and eIF2α+/S51A mice Our transcriptome analyses showed clear transcriptional alterations in hippocampi of 5xFAD compared to wild type mice that were not corrected by the eIF2αS51A allele. Hemizygous 5xFAD mice, which were on a genetic background of B6/SJL, were crossed with eIF2α+/S51A mice (C57BL/6J background), to generate the offspring that was analyzed in the microarray. Hippocampal samples of 12 mice (4 groups: wild-type, 5xFAD, 5xFAD;eIF2α+/S51A and eIF2α+/S51A) were processed using Affymetrix Mouse Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.
2013-09-10 | E-GEOD-50521 | biostudies-arrayexpress
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Project description:Spatial transcriptomics analysis was performed to detect differential gene expression in brain sections of of wild type, 5XFAD mice (model of Alzheimer's Disease), 5XFAD mice treated with either vehicle or human neural stem cells (hNSC)
2023-12-31 | GSE209583 | GEO
Project description:Single cell RNA-seq data were obtained from FACS sorted microglia isolated from different brain regions of 30 weeks old WT and 5xFAD mice to find commonly expressed genes in all clusters.
2020-05-25 | GSE148405 | GEO
Project description:Age-related macular degeneration (AMD) is a leading cause of blindness in the elderly. There are two types of AMD: dry AMD and wet AMD. While laser-induced choroidal neovascularization has been used extensively in the studies of wet AMD by presenting the main features of human wet AMD, there was no established mouse model which fully recapitulates the cardinal features of human dry AMD. In this regard, lack of appropriate mouse model for dry AMD hampered the translational research on the pathogenesis and development of therapeutic agents. We recently suggested that 5XFAD mice could be a mouse model of dry AMD with regard to the amyloid beta (Aβ) related pathology. In this study, using transmission electron microscope, we analyzed ultrastructure of retinal pigment epithelium (RPE) of 5XFAD mice. Of importance, aged 5XFAD mice had ultrastructural changes of RPE and Bruchâs membrane compatible with cardinal features of dry AMD, including loss of apical microvilli and basal infolding of RPE, increased thickness of Bruchâs membrane, basal laminar and linear deposits, and accumulation of lipofuscin granules and undigested photoreceptor outer segment-laiden phagosomes. Using a threshold of 1.2 fold difference, we found â564â differentially expressed genes of which â190â were up-regulated and â374â were down-regulated in the RPE complex of aged 5XFAD mice. These altered genes were implicated in the pathogenesis of AMD including inflammation and immune response-related genes and retinol metabolism-related genes. Taken together, we suggest that aged 5XFAD mice can be used for dry AMD mouse model. All 5XFAD mice used were heterozygotes with respect to the transgene, and non-transgenic wild-type littermate (WT) mice served as controls.
2016-08-10 | E-GEOD-85408 | biostudies-arrayexpress
Project description:Single-nuclei transcriptome sequencing of 5xFAD mouse brain hemisphere with myelin dysfunction
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Project description:State-of-the-art mass spectrometry (MS) methods can comprehensively detect proteomic alterations in neurodegenerative disorders, providing relevant insights unobtainable with transcriptomics investigations. Analyses of the relationship between progressive aggregation and protein abundance changes in brains of 5xFAD transgenic mice have not been reported previously. We quantified progressive A? aggregation in hippocampus and cortex of 5xFAD mice and controls with immunohistochemistry and biochemical membrane filter assays. Protein changes in different mouse tissues were analysed by MS-based proteomics using label-free quantification (LFQ); resulting MS data were processed using an established pipeline. Results were contrasted with existing proteomic data sets from postmortem AD patient brains. Finally, abundance changes in the candidate marker Arl8b were validated in CSF from AD patients and controls using ELISAs. We report a comprehensive biochemical and proteomic investigation of hippocampal and cortical brain tissue derived from 5xFAD transgenic mice, providing a valuable resource to the neuroscientific community. We identified Arl8b, with significant abundance changes in 5xFAD and AD patient brains. Arl8b might enable the measurement of progressive lysosome accumulation in AD patients and have clinical utility as a candidate biomarker.
2023-07-21 | PXD030348 | Pride
Project description:Goals: 1) To analyse amyloid-b aggregation and proteomic and transcriptomic changes in 2, 5 and 8 months old 5xFAD mice 2) To determine differentially expressed proteins correlating and anti-correlating with aggregate formation 3) To analyse whether correlating or anti-correlating proteins change at transcriptional or posttranscriptional level 4) To determine differentially expressed or correlating and anti-correlating proteins which overlap with proteomic changes found in human AD brains 5) To analyse, whether Arl8b, which is an Ab aggregate correlating protein, show significant changes in CSF of AD patients Summary: Our study revealed that Ab42 driven aggregate formation leads to distinct brain region-specific proteome changes in 5xFAD mouse brains. We detected 195 dysregulated proteins correlating or anti-correlating with Ab-aggregation in hippocampus and cortex of 5xFAD mice. Most of these protein changes were caused by posttranscriptional mechanisms, only a minor part was associated with transcriptional dysregulation. A fraction of the Ab-correlated and anti-correlated DEPs was conserved in post-mortem brains of AD patients revealing that proteome changes in 5xFAD mice recapitulate disease-relevant changes in AD patient brains. Among the group of Ab42-correlating proteins, we have found the lysosome associated protein Arl8b, which is present in increased levels in CSF samples of AD patients and might have potential as an AD biomarker.
2023-03-01 | GSE198226 | GEO