ReviewBiomedicines2022
Modeling Alzheimer's Disease in
Review in Biomedicines, 2022. 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, 75 citations in OpenAlex.
- Novel Insights into the Pleiotropic Neuroprotective Action of Synthetic Halogen Free Thyronamine-like Analogues.Molecules (Basel, Switzerland) · 2026Article
- Revealing the Mechanisms of Alzheimer's, Parkinson's and Huntington's Diseases Through Invertebrate Models.Biology · 2026Review
- Sustainable Synthesis of 3-(1H-Indol-3-yl)propionic Acid Derivatives with Anti-Alzheimer Activity.ChemMedChem · 2026Article
- Enzymes of physiological amyloidogenesis control pathological amyloid toxicity.Life science alliance · 2026Article
- A C. elegans model of familial Alzheimer's disease shows age-dependent synaptic degeneration independent of amyloid β-peptide.Neurobiology of disease · 2026Article
- Review
- Leveraging open cheminformatics tools for non-targeted metabolomics analysis of C. elegans: a workflow comparison and application to strains related to xenobiotic metabolism and neurodegeneration.Analytical and bioanalytical chemistry · 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
- Pantoea piersonii IIIF1SW-P2Scientific reports · 2025Article
- SERCA Silencing Alleviates AßInternational journal of molecular sciences · 2025Article
- [Protective effects of escin and dextromethorphan on Alzheimer disease inBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025Article
- Neuroprotective Potential of the Flavonoids Quercetin and Epicatechin in a C. elegans Tauopathy Model.Molecular nutrition & food research · 2025Article
- Structure-based discovery of forsythoside A as an effective inhibitor to reduce the neurotoxicity of amyloid β.Communications chemistry · 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
- Rescue of a Rotenone Model of Parkinson's Disease inInternational journal of molecular sciences · 2025Article
- Unraveling Molecular Targets for Neurodegenerative Diseases ThroughInternational journal of molecular sciences · 2025Review
- Utilization of Artificial Intelligence Coupled with a High-Throughput, High-Content Platform in the Exploration of Neurodevelopmental Toxicity of Individual and Combined PFAS.Journal of xenobiotics · 2025Article
- Article
- Amyloid β induces hormetic-like effects through major stress pathways in a C. elegans model of Alzheimer's Disease.PloS one · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most frequent cause of dementia. After decades of research, we know the importance of the accumulation of protein aggregates such as β-amyloid peptide and phosphorylated tau. We also know that mutations in certain proteins generate early-onset Alzheimer's disease (EOAD), and many other genes modulate the disease in its sporadic form. However, the precise molecular mechanisms underlying AD pathology are still unclear. Because of ethical limitations, we need to use animal models to investigate these processes. The nematode
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.