ReviewDrug discovery today. Technologies2013
Alzheimer's disease drug discovery: in vivo screening using Caenorhabditis elegans as a model for β-amyloid peptide-induced toxicity.
Review in Drug discovery today. Technologies, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 118 citations in OpenAlex.
- A Cerebral Organoid Model of Familial Alzheimer's Disease Using Amyloid Precursor Protein Mutation, Val669Leu (International journal of stem cells · 2026Article
- Fluphenazine, an antipsychotic compound, ameliorates Alzheimer's disease by clearing amyloid beta accumulation in C. elegans.GeroScience · 2026Article
- Iron toxicity potentiates cell-type specific amyloid beta proteotoxicity inbioRxiv : the preprint server for biology · 2026Article
- Metabolites from chia seed (Salvia Hispanica L.) exert antioxidant effects through activation of the DAF-16 pathway and neuroprotective activity in the Caenorhabditis elegans model of Huntington's disease.BMC complementary medicine and therapies · 2026Article
- The amino acid substitutions A30W, K28A, and M35C alter amyloid-β peptide toxicity in cell culture and in anFrontiers in aging neuroscience · 2026Article
- Label-Free Proteomic Profiling of the dvls2 (CL2006) Caenorhabditis elegans Alzheimer's Disease (AD) Model Reveals Conserved Molecular Signatures Shared With the Human AD Brain.Journal of neurochemistry · 2025Article
- Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025Review
- Study on HPLC fingerprint of Saposhnikovia divaricata lipophilic components and anti-aging effects.Scientific reports · 2024Article
- In vivo neuroprotective capacity of a Dunaliella salina extract - comprehensive transcriptomics and metabolomics study.NPJ science of food · 2024Article
- Ethyl acetate extract ofExperimental and therapeutic medicine · 2023Article
- Automated recognition and analysis of body bending behavior in C. elegans.BMC bioinformatics · 2023Article
- Promising Molecular Targets in Pharmacological Therapy for Neuronal Damage in Brain Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Controlling amyloid formation of intrinsically disordered proteins and peptides: slowing down or speeding up?Essays in biochemistry · 2022Article
- LC-MS/MS Insight into Vitamin C Restoration to Metabolic Disorder Evoked by Amyloid β inMetabolites · 2022Article
- Natural Bioactive Products and Alzheimer's Disease Pathology: Lessons fromDiseases (Basel, Switzerland) · 2022Review
- Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans.Nature communications · 2022Article
- 3,6'-disinapoyl sucrose attenuates AβJournal of cellular and molecular medicine · 2022Article
- Orientin Prolongs the Longevity ofOxidative medicine and cellular longevity · 2022Article
- Article
- Label-free photothermal disruption of cytotoxic aggregates rescues pathology in a C. elegans model of Huntington's disease.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a complex human neurodegenerative disease. Currently the therapeutics for AD only treats the symptoms. While numbers of excellent studies have used mammalian models to discover new compounds, the time and effort involved with screening large numbers of candidates is prohibitive. Cultured mammalian neurons are often used to perform high-throughput screens (HTS); however, cell culture lacks the organismal complexity involved in AD. To address these issues several researchers are turning to the roundworm, Caenorhabditis elegans. C. elegans has numerous models of both Tau and Ab induced toxicity, the two prime components observed to correlate with AD pathology. These models have led to the discovery of numerous AD modulating candidates. Further, the ease of performing RNA interference for any gene in the C. elegans genome allows for identification of proteins involved in the mechanism of drug action. These attributes make C. elegans well positioned to aid in the discovery of new AD therapies.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.