ArticleExploration (Beijing, China)2024
The dissolution, reassembly and further clearance of amyloid-β fibrils by tailor-designed dissociable nanosystem for Alzheimer's disease therapy.
Article in Exploration (Beijing, China), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- N 6 -methyladenosine modification regulates cell death in cognitive impairment.Neural regeneration research · 2026Article
- Article
- Research Progress of Lipid Metabolism-Mediated Neuroinflammation in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Review
- Integrating artificial intelligence with nanodiagnostics for early detection and precision management of neurodegenerative diseases.Journal of nanobiotechnology · 2025Review
- Exploring the Neuroprotective Role of Selenium: Implications and Perspectives for Central Nervous System Disorders.Exploration (Beijing, China) · 2025Review
- Nanoplatforms Targeting Intrinsically Disordered Protein Aggregation for Translational Neuroscience Applications.Nanomaterials (Basel, Switzerland) · 2025Review
- Nanomedicine: a cost-effective and powerful platform for managing neurodegenerative diseases.Metabolic brain disease · 2025Review
- Golgi-restored vesicular replenishment retards bone aging and empowers aging bone regeneration.Bone research · 2025Article
- The dissolution, reassembly and further clearance of amyloid-β fibrils by tailor-designed dissociable nanosystem for Alzheimer's disease therapy.Exploration (Beijing, China) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fibrillation of amyloid-β (Aβ) is the critical causal factor in Alzheimer's disease (AD), the dissolution and clearance of which are promising for AD therapy. Although many Aβ inhibitors are developed, their low Aβ-binding affinity results in unsatisfactory effect. To solve this challenge, the Aβ sequence-matching strategy is proposed to tail-design dissociable nanosystem (B6-PNi NPs). Herein, B6-PNi NPs aim to improve Aβ-binding affinity for effective dissolution of amyloid fibrils, as well as to interfere with the in vivo fate of amyloid for Aβ clearance. Results show that B6-PNi NPs decompose into small nanostructures and expose Aβ-binding sites in response to AD microenvironment, and then capture Aβ via multiple interactions, including covalent linkage formed by nucleophilic substitution reaction. Such high Aβ-binding affinity disassembles Aβ fibrils into Aβ monomers, and induces the reassembly of Aβ&nanostructure composite, thereby promoting microglial Aβ phogocytosis/clearance via Aβ receptor-mediated endocytosis. After B6-PNi NPs treatment, the Aβ burden, neuroinflammation and cognitive impairments are relieved in AD transgenic mice. This work provides the Aβ sequence-matching strategy for Aβ inhibitor design in AD treatment, showing meaningful insight in biomedicine.
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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.