ReviewFrontiers in genetics2014
Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases.
Review in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.
What it found
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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
140 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.Neuroscience · 2019Pooled it
- Egg Peptides From American Shad Extend Lifespan and Healthspan in Caenorhabditis elegans via Lipid Metabolism Remodeling and Antioxidant Defense.Chemistry & biodiversity · 2026Article
- Review
- Revealing the Mechanisms of Alzheimer's, Parkinson's and Huntington's Diseases Through Invertebrate Models.Biology · 2026Review
- Functional Analysis of Late-Onset Alzheimer's Disease Risk Genes inbioRxiv : the preprint server for biology · 2026Article
- Cetoleic acid and other long-chain unsaturated fatty acids as neuroprotective nutraceuticals.Lipids in health and disease · 2026Review
- Unlocking neuronal health: leveraging C. elegans for drug repurposing studies.Cell communication and signaling : CCS · 2026Review
- Explosive shock wave exposure leads to age-accelerated motor and sensory decline inbioRxiv : the preprint server for biology · 2025Article
- Attenuation of blood-brain barrier dysfunction by functionalized gold nanoparticles against amyloid-β peptide in an Alzheimer's disease-on-a-chip model.Materials today. Bio · 2025Article
- Presenilin Loss Impairs Synaptic Transmission and Causes Axonal Degeneration through Ryanodine Receptor Dysfunction, Independent of γ-Secretase Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Leaf miRNAs of Withania somnifera Negatively Regulate the Aging-Associated Genes in C. elegans.Molecular neurobiology · 2025Article
- Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025Review
- Honey as a Neuroprotective Agent: Molecular Perspectives on Its Role in Alzheimer's Disease.Nutrients · 2025Review
- High-throughput behavioral screening in Caenorhabditis elegans using machine learning for drug repurposing.Scientific reports · 2025Article
- 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
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- eQTL mapping in transgenic alpha-synuclein carrying Caenorhabditis elegans recombinant inbred lines.Human molecular genetics · 2024Article
- Animal models in neuroscience with alternative approaches: Evolutionary, biomedical, and ethical perspectives.Animal models and experimental medicine · 2024Review
- Cannabinoids and healthy ageing: the potential for extending healthspan and lifespan in preclinical models with an emphasis on Caenorhabditis elegans.GeroScience · 2024Review
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Advances in research and technology has increased our quality of life, allowed us to combat diseases, and achieve increased longevity. Unfortunately, increased longevity is accompanied by a rise in the incidences of age-related diseases such as Alzheimer's disease (AD). AD is the sixth leading cause of death, and one of the leading causes of dementia amongst the aged population in the USA. It is a progressive neurodegenerative disorder, characterized by the prevalence of extracellular Aβ plaques and intracellular neurofibrillary tangles, derived from the proteolysis of the amyloid precursor protein (APP) and the hyperphosphorylation of microtubule-associated protein tau, respectively. Despite years of extensive research, the molecular mechanisms that underlie the pathology of AD remain unclear. Model organisms, such as the nematode, Caenorhabditis elegans, present a complementary approach to addressing these questions. C. elegans has many advantages as a model system to study AD and other neurodegenerative diseases. Like their mammalian counterparts, they have complex biochemical pathways, most of which are conserved. Genes in which mutations are correlated with AD have counterparts in C. elegans, including an APP-related gene, apl-1, a tau homolog, ptl-1, and presenilin homologs, such as sel-12 and hop-1. Since the neuronal connectivity in C. elegans has already been established, C. elegans is also advantageous in modeling learning and memory impairments seen during AD. This article addresses the insights C. elegans provide in studying AD and other neurodegenerative diseases. Additionally, we explore the advantages and drawbacks associated with using this model.
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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.