Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease - Wikidata - wikimedia - TriplyDB

Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease

Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease

http://www.wikidata.org/entity/Q36460071

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Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases Drug repositioning approaches for the discovery of new therapeutics for Alzheimer's disease C. elegans in high-throughput drug discovery The struggle by Caenorhabditis elegans to maintain proteostasis during aging and disease Complex regulation of γ-secretase: from obligatory to modulatory subunits Systematic development of small molecules to inhibit specific microscopic steps of Aβ42 aggregation in Alzheimer's disease A semi-automated motion-tracking analysis of locomotion speed in the C. elegans transgenics overexpressing beta-amyloid in neurons.Systems biology approach to late-onset Alzheimer's disease genome-wide association study identifies novel candidate genes validated using brain expression data and Caenorhabditis elegans experiments.Caenorhabditis elegans: a model to investigate oxidative stress and metal dyshomeostasis in Parkinson's disease Genetic variation in neurodegenerative diseases and its accessibility in the model organism Caenorhabditis elegans.Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease The γ-secretase complex: from structure to function.Clioquinol promotes the degradation of metal-dependent amyloid-β (Aβ) oligomers to restore endocytosis and ameliorate Aβ toxicity.Therapeutic targeting of misfolding and conformational change in α1-antitrypsin deficiency.A γ-Secretase Independent Role for Presenilin in Calcium Homeostasis Impacts Mitochondrial Function and Morphology in Caenorhabditis elegans.An anticancer drug suppresses the primary nucleation reaction that initiates the production of the toxic Aβ42 aggregates linked with Alzheimer's disease.Modeling Alzheimer's disease: from past to future Energy crisis precedes global metabolic failure in a novel Caenorhabditis elegans Alzheimer Disease model.Worming our way to novel drug discovery with the Caenorhabditis elegans proteostasis network, stress response and insulin-signaling pathways.Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases.Enhanced toxicity of silver nanoparticles in transgenic Caenorhabditis elegans expressing amyloidogenic proteins.Biochemically-defined pools of amyloid-β in sporadic Alzheimer's disease: correlation with amyloid PET.Selective targeting of primary and secondary nucleation pathways in Aβ42 aggregation using a rational antibody scanning method.Immunohistochemical analysis reveals variations in proteasome tissue expression in C. elegans In vitro aggregating β-lactamase-polyQ chimeras do not induce toxic effects in an in vivo Caenorhabditis elegans model.Age-Dependent Protein Aggregation Initiates Amyloid-β Aggregation.Polyphosphate: A Conserved Modifier of Amyloidogenic Processes.Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity.Dihydropyrimidine-Thiones and Clioquinol Synergize To Target β-Amyloid Cellular Pathologies through a Metal-Dependent Mechanism.Metformin Attenuates Aβ Pathology Mediated Through Levamisole Sensitive Nicotinic Acetylcholine Receptors in a C. elegans Model of Alzheimer's Disease.Fucoidan inhibits amyloid-β-induced toxicity in transgenic Caenorhabditis elegans by reducing the accumulation of amyloid-β and decreasing the production of reactive oxygen species.The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade.Nuclear Export Inhibition Enhances HLH-30/TFEB Activity, Autophagy, and Lifespan.Presenilin mutations deregulate mitochondrial Ca homeostasis and metabolic activity causing neurodegeneration in Role of Presenilin in Mitochondrial Oxidative Stress and Neurodegeneration in

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Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease

http://www.wikidata.org/entity/Q36460071

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Molecular Neurodegeneration

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Christopher D Link

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Kevin J Barnham

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Robert A Cherny

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The genetics of Caenorhabditis elegans

Amyloid plaque core protein in Alzheimer disease and Down syndrome

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

Stabilization of neurotoxic soluble beta-sheet-rich conformations of the Alzheimer's disease amyloid-beta peptide

Improved prediction of signal peptides: SignalP 3.0

Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1

Two-sided confidence intervals for the single proportion: comparison of seven methods

Alzheimer's disease: the amyloid cascade hypothesis

Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease

daf-16 integrates developmental and environmental inputs to mediate aging in the nematode Caenorhabditis elegans

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Colin L. Masters

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Alzheimer's disease

Caenorhabditis elegans

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3519830

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