Project description:the study aims to describe the modifications occurring the microglia isolated from mouse models of 2 lysosomal storage diseases: Mucolipidosis type 4 and fabry disease.
Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.
Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.
Project description:We subjected old (21-22 month) and young (3-4 month) male C57BL/6 mice to 45 min transient oclusion of the middle cerebral artery and obtained the brain four days later. We obtained bodipy+ microglia from the ischemic brain tissue by FACS.
Project description:To look for age-related changes in the liver, we used RNAseq gene expression analysis to characterize mRNA expression profile in livers from 1-month vs. 6-month-old mice
Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.
Project description:Fabry nephropathy (FN) is a rare disorder caused by mutations in the alpha-galactosidase A gene. In this study we aim at providing a framework allowing selection of biomarkers and drug-targets. Two independent Fabry Nephropathy cohorts (FA.NO and CH.RO) were subjected to RNAseq from archival kidney biopsies taken prior and up to 10 years of Enzyme Replacement Therapy. Four compartments were laser capture microdissected (glomeruli, proximal tubuli, distal tubuli and arteries). We found several pathways that were consistently altered and that these kidney compartments’ transcriptional landscapes can be leveraged in the search for drug-targets and biomarkers.