MRNA and miRNA expression in parietal lobe cortex in Alzheimer's disease
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE16759 | GEO | 2010/01/31
SECONDARY ACCESSION(S): PRJNA117471
REPOSITORIES: GEO
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Project description:In this study, we jointly profiled mRNA and miRNA expression to determine the role of miRNAs in AD, and whether the levels of miRNAs are related to those of target mRNAs. We found a bias towards positive correlation between levels of miRNAs and those of their targets. We profiled parietal lobe tissue from 4 AD patients and 4 age-matched controls.
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Project description:MicroRNAs influence restorative physiological or degenerative pathological processes in several neurological disorders, yet their role in AlzheimerM-bM-^@M-^Ys disease remains unclear. Here we compared microRNAs expression in the period of AD pathogenesis when mice first begin to have detectable extracellular AM-NM-2 deposition. Tg2576 mice aged 9-10 months and their wild type littermates, as well as a double transgenic model of AD, APP/ PS1M146V/+ and wild type C57BL/6J mice both at 3-4 age months (n=3) were used. Hippocampus tissue miRNAs were detected by hybridization to microarrays having 924 mammalian miRNA probes.The result indicated that some of the deregulated miRNAs in AD mice have been implicated in amyloid beta production. AD mice vs. control mice
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Project description:Alzheimer’s disease (AD) is a neurodegenerative disease displaying plaques formed by the neurotoxic amyloid β-peptide (Aβ), and intracellular neurofibrillary tangles consisting of protein tau. However, how these pathologies relates to the massive neuronal death that occurs in AD brains remain elusive. Neprilysin is the major A degrading enzyme and a lack thereof increases A levels in the brain twofold. To identify altered protein expression levels induced by increased Aβ levels, we performed a proteomic analysis of the brain of the AD mouse model APPsw and compared it to that of APPsw mice lacking neprilysin. To this end we established an LC-MS/MS method to analyze brain homogenate, using an 18O-labeled internal standard to accurately quantify the protein levels. To distinguish between alterations in protein levels directly caused by increased A levels and those induced by neprilysin deficiency independently of A, the brain proteome of neprilysin deficient APPsw mice was compared to that of neprilysin deficient mice. By this approach we identified approximately 600 proteins and could quantify the levels of 300 of these. Pathway analysis showed that many of the proteins with altered expression were involved in neurological disorders, and that tau, presenilin and APP were key regulators in the identified networks. The data have been deposited to the ProteomeXchange Consortium with identifier PXD000968. Interestingly, the levels of several proteins, including some not previously reported to be associated with AD, were associated with increased A levels.
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Project description:MicroRNAs influence restorative physiological or degenerative pathological processes in several neurological disorders, yet their role in Alzheimer’s disease remains unclear. Here we compared microRNAs expression in the period of AD pathogenesis when mice first begin to have detectable extracellular Aβ deposition. Tg2576 mice aged 9-10 months and their wild type littermates, as well as a double transgenic model of AD, APP/ PS1M146V/+ and wild type C57BL/6J mice both at 3-4 age months (n=3) were used. Hippocampus tissue miRNAs were detected by hybridization to microarrays having 924 mammalian miRNA probes.The result indicated that some of the deregulated miRNAs in AD mice have been implicated in amyloid beta production.
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