ArticleFrontiers in pharmacology2019
Experimental Pharmacology in Transgenic Rodent Models of Alzheimer's Disease.
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed.
- Review
- Muscarinic Receptors and Alzheimer's Disease: New Perspectives and Mechanisms.Current issues in molecular biology · 2024Review
- Rodent Models of Alzheimer's Disease: Past Misconceptions and Future Prospects.International journal of molecular sciences · 2024Review
- Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity.NeuroSci · 2023Article
- Protective Effects of Dendrobium nobile Lindl. Alkaloids on Alzheimer's Disease-like Symptoms Induced by High-methionine Diet.Current neuropharmacology · 2022Article
- Obesity Prevents S-Adenosylmethionine-Mediated Improvements in Age-Related Peripheral and Hippocampal Outcomes.Nutrients · 2021Article
- The aging endothelium.Vascular biology (Bristol, England) · 2021Review
- Ted Sourkes, Moussa Youdim and I.Journal of neural transmission (Vienna, Austria : 1996) · 2020Article
- Neuronal-Glial Interaction in a Triple-Transgenic Mouse Model of Alzheimer's Disease: Gene Ontology and Lithium Pathways.Frontiers in neuroscience · 2020Article
- Altered expression of Notch1 in Alzheimer's disease.PloS one · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
This Mini Review discusses the merits and shortfalls of transgenic (tg) rodents modeling aspects of the human Alzheimer's disease (AD) pathology and their application to evaluate experimental therapeutics. It addresses some of the differences between mouse and rat tg models for these investigations. It relates, in a condensed fashion, the experience of our research laboratory with the application of anti-inflammatory compounds and S-adenosylmethionine (SAM) at the earliest stages of AD-like amyloid pathology in tg mice. The application of SAM was intended to revert the global brain DNA hypomethylation unleashed by the intraneuronal accumulation of amyloid-β-immunoreactive material, an intervention that restored levels of DNA methylation including of the
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