ArticleNeuroreport2018
Glutathione-mimetic D609 alleviates memory deficits and reduces amyloid-β deposition in an AβPP/PS1 transgenic mouse model.
Article in Neuroreport, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Neuroprotective potential of biochanin-A and review of the molecular mechanisms involved.Molecular biology reports · 2023Review
- A Diet Containing Rutin Ameliorates Brain Intracellular Redox Homeostasis in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Neuronal glutathione loss leads to neurodegeneration involving gasdermin activation.Scientific reports · 2023Article
- Non-Enzymatic Antioxidants against Alzheimer's Disease: Prevention, Diagnosis and Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- Orally Bioavailable Prodrugs of ψ-GSH: A Potential Treatment for Alzheimer's Disease.Journal of medicinal chemistry · 2022Article
- Tricyclodecan-9-yl-Xanthogenate (D609): Mechanism of Action and Pharmacological Applications.International journal of molecular sciences · 2022Review
- Molecular Mechanisms and Genetics of Oxidative Stress in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive extracellular deposition of amyloid-β-peptide (Aβ) in the brain is a pathological hallmark of Alzheimer's disease (AD). Oxidative stress is associated with the onset and progression of AD and contributes to Aβ generation. Tricyclodecan-9-yl-xanthogenate (D609) is a glutathione (GSH)-mimetic compound. Although the antioxidant properties of D609 have been well-studied, its potential therapeutic significance on AD remains unclear. In the present study, we used a mouse model of AD to investigate the effects and the mechanism of action of D609 on AD. We found that D609 treatment significantly improved the spatial learning and alleviated the memory decline in the mice harboring amyloid precursor protein (APP) and presenilin-1 (PS1) double mutations (AβPP/PS1 mice). D609 treatment also increased GSH level, GSH and oxidative glutathione ratio, and superoxide dismutase activity, whereas decreased malondialdehyde and protein carbonyl levels, suggesting that D609 alleviated oxidative stress in AβPP/PS1 mice. In addition, D609 reduced β-secretase 1 level and decreased amyloidogenic processing of AβPP, consequently reducing Aβ deposition in the mice. Thus, our findings suggest that D609 might produce beneficial effects on the prevention and treatment of AD.
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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.