ReviewBrain structure & function2010
Understanding the molecular basis of Alzheimer's disease using a Caenorhabditis elegans model system.
Review in Brain structure & function, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 66 citations in OpenAlex.
- MINERVA: a public XAI-powered platform advancing multi-target discovery in Alzheimer's disease.Journal of cheminformatics · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
- DMT1 knockout abolishes ferroptosis induced mitochondrial dysfunction in C. elegans amyloid β proteotoxicity.Free radical biology & medicine · 2024Article
- Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.Nucleic acids research · 2024Article
- DMT1 knockout abolishes ferroptosis induced mitochondrial dysfunction inbioRxiv : the preprint server for biology · 2024Article
- Clearance of extracellular human amyloid-β aggregates inmicroPublication biology · 2024Article
- Switching On/Off Amyloid Plaque Formation in Transgenic Animal Models of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Article
- Zn-dependent β-amyloid Aggregation and its Reversal by the Tetrapeptide HAEE.Aging and disease · 2023Article
- Promising Molecular Targets in Pharmacological Therapy for Neuronal Damage in Brain Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Exendin-4 alleviates β-Amyloid peptide toxicityFrontiers in aging neuroscience · 2022Article
- Article
- Subcritical Water Extraction ofMolecules (Basel, Switzerland) · 2021Article
- The Role of CaCells · 2020Review
- Modulation of the Aβ-Peptide-Aggregation Pathway by Active Compounds FromFrontiers in aging neuroscience · 2020Article
- Ageing as a risk factor for neurodegenerative disease.Nature reviews. Neurology · 2019Review
- Ingredients in Zijuan Pu'er Tea Extract Alleviate β-Amyloid Peptide Toxicity in aMolecules (Basel, Switzerland) · 2019Article
- Caenorhabditis elegans hub genes that respond to amyloid beta are homologs of genes involved in human Alzheimer's disease.PloS one · 2019Article
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 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the major cause of dementia in the United States. At the cellular level, the brains of AD patients are characterized by extracellular dense plaques and intracellular neurofibrillary tangles whose major components are the beta-amyloid peptide and tau, respectively. The beta-amyloid peptide is a cleavage product of the amyloid precursor protein (APP); mutations in APP have been correlated with a small number of cases of familial Alzheimer's disease. APP is the canonical member of the APP family, whose functions remain unclear. The nematode Caenorhabditis elegans, one of the premier genetic workhorses, is being used in a variety of ways to address the functions of APP and determine how the beta-amyloid peptide and tau can induce toxicity. First, the function of the C. elegans APP-related gene, apl-1, is being examined. Although different organisms may use APP and related proteins, such as APL-1, in different functional contexts, the pathways in which they function and the molecules with which they interact are usually conserved. Second, components of the gamma-secretase complex and their respective functions are being revealed through genetic analyses in C. elegans. Third, to address questions of toxicity, onset of degeneration, and protective mechanisms, different human beta-amyloid peptide and tau variants are being introduced into C. elegans and the resultant transgenic lines examined. Here, we summarize how a simple system such as C. elegans can be used as a model to understand APP function and suppression of beta-amyloid peptide and tau toxicity in higher organisms.
Indexed as
Identifiers
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.