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
Similar Datasets
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.
2010-01-30 | E-GEOD-16759 | biostudies-arrayexpress
Project description:Cognitively normal brains are compared to sporadic AD and Down syndrome brains with AD for comparison of two different forms of Alzheimer's disease
2024-06-30 | E-MTAB-14179 | biostudies-arrayexpress
Project description:Sustained anxiety is a key symptom of anxiety disorders and may be associated with neural activation in the right inferior parietal lobe (rIPL), particularly under unpredictable threat. This finding suggests a moderating role of the rIPL in sustained anxiety, which we tested in the current study. We applied cathodal or sham transcranial direct current stimulation (tDCS) to the rIPL as a symptom provocation method in 22 healthy participants in a randomized, double-blind, crossover study, prior to two recordings of cerebral blood flow (CBF). In between, we applied a threat-of-shock paradigm with three conditions: unpredictable (U), predictable (P), or no electric shocks (N). We hypothesized increased anxiety under U, but not under P or N. Furthermore, we expected reduced CBF in the rIPL after tDCS compared to sham. As predicted, anxiety was higher in the U than the P and N conditions, and active tDCS augmented this effect. While tDCS did not alter CBF in the rIPL, it did attenuate the observed increase in brain regions that typically increase activation as a response to anxiety. These findings suggest that the rIPL moderates sustained anxiety as a gateway to brain regions crucial in anxiety. Alternatively, anodal tDCS over the left orbitofrontal cortex (lOFC) may have increased anxiety through disruption of OFC-amygdala interactions.
| S-EPMC7214722 | biostudies-literature
Project description:We quantified genome-wide levels of H3K27ac in post-mortem entorhinal cortex tissue samples, identifying widespread Alzheimer's disease (AD)-associated acetylomic variation. Differentially acetylated peaks were identified in the vicinity genes implicated in both tau and amyloid neuropathology (MAPT, APP, PSEN1, PSEN2), as well as genomic regions containing variants associated with sporadic late-onset AD (CR1, TOMM40). Both MAPT and PSEN2 are characterized by an extended hyperacetylated region upstream of the TSS mapping to enhancers in the brain. We show that genes annotated to AD-associated hyper- and hypoacetylated peaks are enriched for brain- and neuropathology-related functions.
2018-08-11 | GSE102538 | GEO
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
2013-09-19 | E-GEOD-48028 | biostudies-arrayexpress
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.
2015-07-29 | PXD001786 | Pride
Project description:The libraries contained in this experiment come from human fetal parietal lobe tissue from independent donors. They are stranded PE101 Illumina Hi-Seq RAMPAGE libraries from rRNA-depleted Total RNA > 200 nucleotides in size. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2016-11-08 | GSE87932 | GEO
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.
2013-09-19 | GSE48028 | GEO
Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease. We prepared RNA samples from the gray matter of frontal and temporal cortices and hippocampi derived from 88 postmortem brains, among which 26 cases were pathologically diagnosed as having AD or an AD-like disorder. High-quality RNA (RIN≧6.9) samples were subjected to microarray analysis using the Affymetrix Human Gene 1.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 1.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 33 frontal cortex samples, among which 15 were from AD patients; 29 temporal cortex samples, among which 10 were from AD patients; 17 hippocampus samples, among which seven were from AD patients
2013-04-17 | E-GEOD-36980 | biostudies-arrayexpress
Project description:Contingency awareness is thought to rely on an intact medial temporal lobe and also appears to be a function of age, as older subjects tend to be less aware. The current investigation used functional magnetic resonance imaging, transcranial direct current stimulation, and eyeblink classical conditioning to study brain processes related to contingency awareness as a function of age. Older adults were significantly less aware of the relationship between the tone-airpuff pairings than younger adults. Greater right parietal functional magnetic resonance imaging activation was associated with higher levels of contingency awareness for younger and older subjects. Cathodal transcranial direct current stimulation over the right parietal lobe led to lower levels of awareness in younger subjects without disrupting conditioned responses. Older adults exhibited hyperactivations in the parietal and medial temporal lobes, despite showing no conditioning deficits. These findings strongly support the idea that the parietal cortex serves as a substrate for contingency awareness and that age-related disruption of this region is sufficient to impair awareness, which may be a manifestation of some form of naturally occurring age-related neglect.
| S-EPMC7953809 | biostudies-literature