ArticleInternational journal of molecular sciences2022
Amentoflavone Promotes Cellular Uptake and Degradation of Amyloid-Beta in Neuronal Cells.
Article in International journal of molecular sciences, 2022. 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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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Biophysical and Computational Insights into Alpha-1 Antitrypsin Aggregation and Its Inhibition by Natural Polyphenols.Biomedicines · 2026Article
- Unlocking the Neuroprotective Potential ofAntioxidants (Basel, Switzerland) · 2026Review
- Potential of phytochemicals in the treatment of Alzheimer disease by modulating lysosomal dysfunction: a systematic review.Chinese medicine · 2025Review
- AβInternational journal of molecular sciences · 2025Article
- Connectome-based biophysical models of pathological protein spreading in neurodegenerative diseases.PLoS computational biology · 2025Review
- Nanotechnology for microglial targeting and inhibition of neuroinflammation underlying Alzheimer's pathology.Translational neurodegeneration · 2024Article
- Unraveling Amentoflavone's Therapeutic Potential in Alzheimer's Disease: A Preclinical Assessment.Combinatorial chemistry & high throughput screening · 2024Review
- Amentoflavone for treating cardiocerebrovascular diseases and neurological disorders.Frontiers in pharmacology · 2024Review
- A Comparative Analysis of Radical Scavenging, Antifungal and Enzyme Inhibition Activity of 3'-8″-Biflavones and Their Monomeric Subunits.Antioxidants (Basel, Switzerland) · 2023Article
- Photobiomodulation in Alzheimer's Disease-A Complementary Method to State-of-the-Art Pharmaceutical Formulations and Nanomedicine?Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deposition of fibrillar forms of amyloid β-protein (Aβ) is commonly found in patients with Alzheimer's disease (AD) associated with cognitive decline. Impaired clearance of Aβ species is thought to be a major cause of late-onset sporadic AD. Aβ secreted into the extracellular milieu can be cleared from the brain through multiple pathways, including cellular uptake in neuronal and non-neuronal cells. Recent studies have showed that the naturally-occurring polyphenol amentoflavone (AMF) exerts anti-amyloidogenic effects. However, its effects on metabolism and cellular clearance of Aβ remain to be tested. In the present study, we demonstrated that AMF significantly increased the cellular uptake of both Aβ
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