Project description:The specific miRNAs were altered in the brain of senescense-accerelated mouse prone 8 (SAMP8) compered with age-matched senescence-accerelated mouse resistant 1 (SAMR1).
Project description:Histopathological changes occur in the brainstem during the early stages of Alzheimer's disease (AD), with the pathological changes of the brain lesions ascending progressively in accordance with the Braak staging system. The senescence‑accelerated mouse prone 8 (SAMP8) mouse model has been previously used as a model of age‑dependent neurodegenerative diseases, including AD. In the present study, microRNAs (miRNAs) that were upregulated or downregulated in SAMP8 brainstems were identified using miRNA profiling of samples obtained from miRNA arrays. The preliminary stage of cognitive dysfunction was examined using male 5‑month‑old SAMP8 mice, with age‑matched senescence‑accelerated mouse resistant 1 mice as controls. A Y‑maze alternation test was performed to assess short‑term working memory and miRNA profiling was performed in each region of the dissected brain (brainstem, hippocampus and cerebral cortex). SAMP8 mice tended to be hyperactive, but short‑term working memory was preserved. Two miRNAs were upregulated (miR‑491‑5p and miR‑764‑5p) and two were downregulated (miR‑30e‑3p and miR‑323‑3p) in SAMP8 brainstems. In SAMP8 mice, the expression level of upregulated miRNAs were the highest in the brainstem, wherein age‑related brain degeneration occurs early. It was demonstrated that the order of specific miRNA expression levels corresponded to the progression order of age‑related brain degeneration. Differentially expressed miRNAs regulate multiple processes, including neuronal cell death and neuron formation. Changes in miRNA expression may result in the induction of target proteins during the early stages of neurodegeneration in the brainstem. These findings suggest that studying altered miRNA expression may provide molecular evidence for early age‑related neuropathological changes.
Project description:Macrophage aging is pathogenic in numerous age-associated diseases, including age-related macular degeneration. The purpose of this experiment was to profile microRNA expression in young and aged macrophages at baseline and in response to oxLDL and acLDL.
Project description:This SuperSeries is composed of the following subset Series: GSE28002: Gene expression of the whole mouse eye GSE28032: Epigenetic Regulation of IL17RC in Age-related Macular Degeneration (MeDIP-chip) Refer to individual Series
Project description:To investigate the roles of microRNAs in the aqueous humor of patients with typical age-related macular degeneration and polypoidal choroidal vasculopathy using next-generation sequencing.
Project description:We profiled using single cell RNA sequencing the peripheral blood mononuclear cells from control patients and patients with age-related macular degeneration (AMD).
Project description:Illumina Infinium HumanMethylation450 BeadChip data from genomic DNA of retinal pigment epithelium from Age-related Macular Degeneration patients or age-matched controls.
Project description:Macrophage aging is pathogenic in numerous diseases, including age-related macular degeneration. Although prior studies have explored the functional consequences of macrophage aging, less is known about its cellular basis or what defines the transition from physiologic aging to disease. The purpose of this experiment was to characterize the transcriptomic changes associated with macrophage aging.
Project description:Age-related macular degeneration has a strong epidemiological association with cardiovascular disease. One pathogenic hypothesis that applies to both diseases is the concept of an abnormal cellular response to injury resulting in a disease phenotype. It has been hypothesized that this phenotype is also present in dermal fibroblasts. This study tests this hypothesis by examination of the expression profiles of fibroblasts obtained from diseased patients and subjected to sublethal cell injury.