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Beta Amyloid toxicity in a Caenorhabditis elegans model of Alzheimer's disease

ABSTRACT: Transgenic animals were engineered to express human amyloid peptide controlled by a muscle-specific, heat-inducible promoter. At low temperatures (16°C) Abeta expression is minimal, while at higher temperatures (20-25°C) Abeta accummulates in large quantities and causes paralysis. GFP- and GFP::degron (a toxic aggregating GFP mutant)-expressing animals were used as controls.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE65851 | GEO | 2015/02/12

SECONDARY ACCESSION(S): PRJNA275227

REPOSITORIES: GEO

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Beta Amyloid toxicity in a Caenorhabditis elegans model of Alzheimer's disease

Project description:Transgenic animals were engineered to express human amyloid peptide controlled by a muscle-specific, heat-inducible promoter. At low temperatures (16°C) Abeta expression is minimal, while at higher temperatures (20-25°C) Abeta accummulates in large quantities and causes paralysis. GFP- and GFP::degron (a toxic aggregating GFP mutant)-expressing animals were used as controls. Animals were grown at 16°C till early 3rd larval stage and then upshifted to 25°C. Animals were harvested at the time of upshift (T0), and every 4 hours later until 20 hours postupshift (T4-T20).

2015-02-12 | E-GEOD-65851 | biostudies-arrayexpress

Amyloid-beta Citrullination in Alzheimer's Disease

Project description:Amyloid-beta peptides which aggregate and accumulate in Alzheimer’s disease (AD) brain are known to have sequential N-terminal truncations and multiple post-translational modifications (PTM) such as isomerization, pyroglutamate formation, phosphorylation, nitration and dityrosine cross-linking. Here we add to the list of PTM citrullination (deimination) of Arg5 residue in plaque-derived Abeta in sporadic AD brains, identified by tandem mass spectrometry. We quantitated the level of citrullination on multiple N-truncated Abeta isoforms present in plaque-associated fractions and found that almost 30 % of pyroGlu3-Abeta pool was citrullinated in plaques from AD temporal cortex. We also documented citrullinated Abeta peptides in the detergent insoluble fractions from AD frontal cortex with ~ 22 % citrullination in the pyroGlu3-Abeta pool. Citrullination of Abeta is a common PTM, closely associated with pyroglutamate-Abeta formation and Abeta accumulation in AD. This may have implications for Abeta toxicity, auto-antigenicity of Abeta, and may be relevant for the design of diagnostic assays and therapeutic targeting.

2021-11-24 | PXD025620 | Pride

Microarray analysis of gene expression profiles in human neuroblastoma cells exposed to Amyloid beta-Zn and Amyloid beta-Cu complexes

Project description:Abnormal metal accumulation is associated with Alzheimer’s disease (AD) and has a relevant role in affecting amyloid beta-peptide (Abeta) aggregation and neurotoxicity.In the present study, employing a microarray analysis of 35,129 genes, we analyzed gene expression profile changes due to exposure to Abeta-Zn or Abeta-Cu complexes in neuronal-like cells (SH-SY5Y). Microarray data indicated that Abeta-Zn or Abeta-Cu complexes selectively alter expression of genes mainly related to cell death, inflammatory responses, and apoptosis.Taken together these findings indicate that Abeta-Zn or Abeta-Cu show some commonalities in affecting AD-related target functions. The overall modulatory activity on these genes supports the idea of a possible net result leading to mechanisms that counteract toxic effects of Abeta-Zn or Abeta-Cu.

2012-05-01 | GSE37661 | GEO

TALEN Editing of APP Gene in WiCell WA09 (H9) Cells to directly express amyloid beta proteins

Project description:We used TALEN editing to insert a direct expression cassette of either Abeta42 or Abeta 40 eliminating any requirement for amyloidogenic processing of APP to produce Abeta.

2018-12-31 | GSE119527 | GEO

Alzheimer's disease proteomics

Project description:This project aims to determine how the brain proteome is remodeled in Alzheimer's disease (AD). AD is pathologically characterized by an accumulation of insoluble aggregates composed of Abeta peptides in the brain and is clinically characterized by progressive memory impairment. While the precise pathogenic mechanism(s) that drive AD remain unclear, synapse loss is a pathological hallmark and correlates with cognitive decline. Abeta peptides accumulate due in large part to perturbed protein degradation pathways, and increasing evidence shows that Abeta peptides impair multiple cellular pathways. To advance our understanding of these complex processes we have completed a comprehensive proteomic characterization of the three different AD mouse models before and after the onset of pathology.

2016-12-19 | MSV000080431 | MassIVE

Comparative profiling of cortical gene expression in Alzheimer's disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation

Project description:Alzheimer's disease (AD) is the most common form of dementia, characterized by accumulation of amyloid beta (Abeta) and neurofibrillary tangles. Oxidative stress and inflammation are considered to play an important role in the development and progression of AD. However, the extent to which these events contribute to the Abeta pathologies remains unclear. We performed inter-species comparative gene expression profiling between AD patient brains and the App (NL-G-F/NL-G-F) and 3xTg-AD-H mouse models. Genes commonly altered in App (NL-G-F/NL-G-F) and human AD cortices correlated with the inflammatory response or immunological disease. Among them, expression of AD-related genes (C4a/C4b, Cd74, Ctss, Gfap, Nfe2l2, Phyhd1, S100b, Tf, Tgfbr2, and Vim) was increased in the App (NL-G-F/NL-G-F) cortex as Abeta amyloidosis progressed with exacerbated gliosis, while genes commonly altered in the 3xTg-AD-H and human AD cortices correlated with neurological disease. The App (NL-G-F/NL-G-F) cortex also had altered expression of genes (Abi3, Apoe, Bin2, Cd33, Ctsc, Dock2, Fcer1g, Frmd6, Hck, Inpp5D, Ly86, Plcg2, Trem2, Tyrobp) defined as risk factors for AD by genome-wide association study or identified as genetic nodes in late-onset AD. These results suggest a strong correlation between cortical Abeta amyloidosis and the neuroinflammatory response and provide a better understanding of the involvement of gender effects in the development of AD.

2017-12-21 | GSE92926 | GEO

Cold acclimation

Project description:Experiment was designed to identify transcriptome changes during cold acclimation of Drosophila melanogaster male flies. Resistance to cold is often measured by recovery times from chill coma, which is induced almost immediately upon exposure to low but non-freezing temperatures (~0C), with flies becoming immobilised and losing motor activity. This paralysis is also ostensibly reversible upon return to normal temperatures, although again there can be longer term effects. Acclimation for increased cold resistance requires exposure periods ranging from hours or days to several weeks at low temperatures between 0C to 12C, and samples were taken during the cold acclimation period (1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 36 hr and 48 hr).

2014-05-01 | E-MTAB-1607 | biostudies-arrayexpress

Comprehensive phosphoproteome analysis unravels the core signaling network that initiates the earliest synapse pathology in preclinical Alzheimer's disease brain

Project description:Using a high-end mass spectrometry, we screened phosphoproteins and phosphopeptides in four types of Alzheimer's disease (AD) mouse models and human AD postmortem brains. We identified commonly changed phosphoproteins in multiple models and also determined phosphoproteins related to initiation of Abeta deposition in the mouse brain. We put the proteins on experimentally verified protein-protein interaction databases. Surprisingly most of the core phosphoproteins were directly connected, and they formed a functional network linked to synaptic spine formation. The change of the core network started at a preclinical stage even before histological Abeta deposition. Systems biology analyses suggested phosphorylation of MARCKS by over-activated kinases including PKCs and CaMKs initiates synapse pathology.

2014-09-10 | PXD001292 | Pride

Heat Hardening

Project description:A common measure of heat resistance in Drosophila is the time it takes a fly to be knocked down by higher temperatures measured in a long knockdown tube or in small glass vials. This heat knockdown process involves gradual paralysis and non-responsiveness to stimuli, usually within half hour duration of constant heat exposure, and is ostensibly reversible upon return to lower temperatures, although there may be long-term fitness effects. Hardening for increased heat resistance requires exposure periods of up to 3 hours at temperatures ranging from 34C to 38C. The experiment was aimed at understanding the heat hardening process and samples were taken during the hardening period (15 minutes, 45 minutes, 1½ hours, 2¼ hours and 3 hours).

2014-05-01 | E-MTAB-1608 | biostudies-arrayexpress

Abeta levels in APP Tg mice with mixed genetic backgrounds

Project description:We combined a mouse model of Abeta accumulation and transcriptomics, and identified Klc1 as an Abeta accumulation modifier in vivo.

2014-01-15 | GSE40330 | GEO

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