ArticleAlzheimer's research & therapy2019
Rescue of cognitive deficits in APP/PS1 mice by accelerating the aggregation of β-amyloid peptide.
Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Polyphenolic Imidazopyridines as Multifunctional Modulators of Oxidative Stress, Metal Dyshomeostasis, and βAntioxidants (Basel, Switzerland) · 2026Article
- Amyloid Plaques Ameliorate Memory Deficits and Hippocampal Neuron Loss in an Aβ4-42-Driven Alzheimer's Disease Mouse Model.Molecular neurobiology · 2026Article
- Current perspective on amyloid aggregation accelerating properties of the artificial butter flavoring, diacetyl.Neural regeneration research · 2024Article
- Early Life Stress Enhances Cognitive Decline and Alters Synapse Function and Interneuron Numbers in Young Male APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2023Article
- Age, sex, and cerebral microbleeds in EFAD Alzheimer disease mice.Neurobiology of aging · 2021Article
- Losartan Improves Memory, Neurogenesis and Cell Motility in Transgenic Alzheimer's Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundBrain amyloid deposition is one of the main pathological characteristics of Alzheimer's disease (AD). Soluble oligomers formed during the process that causes β-amyloid (Aβ) to aggregate into plaques are considered to have major neurotoxicity. Currently, drug development for the treatment of Alzheimer's disease has encountered serious difficulties. Our newly proposed solution is to accelerate the aggregation of Aβ to reduce the amount of cytotoxic Aβ oligomers in brain tissue. This strategy differs from the existing strategy of reducing the total Aβ content and the number of amyloid plaques.
methodIn this study, we screened a small library and found that a flavonoid compound (ZGM1) promoted the aggregation of β-amyloid (Aβ). We further verified the binding of ZGM1 to Aβ42 using a microscale thermophoresis (MST) assay. Subsequently, we used dot blotting (DB), transmission electron microscopy (TEM), and thioflavin T fluorescence (ThT) measurements to study the aggregation of Aβ under the influence of ZGM1. By using cell experiments, we determined whether ZGM1 can inhibit the cytotoxicity of Aβ. Finally, we studied the protective effects of ZGM1 on cognitive function in APPswe/PS1 mice via behavioral experiments and measured the number of plaques in the mouse brain by thioflavin staining.
resultsZGM1 can bind with Aβ directly and mediate a new Aβ assembly process to form reticular aggregates and reduce the amount of Aβ oligomers. Animal experiments showed that ZGM1 can significantly improve cognitive dysfunction and that Aβ plaque deposition in the brain tissue of mice in the drug-administered group was significantly increased.
conclusionOur research suggests that promoting Aβ aggregation is a promising treatment method for AD and deserves further investigation.
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