ArticleBiophysical journal2020
Endocytosis Is a Key Mode of Interaction between Extracellular β-Amyloid and the Cell Membrane.
Article in Biophysical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Protein Misfolding in the Pathogenesis and Diagnosis of Neurodegenerative Diseases (Review).Sovremennye tekhnologii v meditsine · 2025Review
- Mechanical stimulation prevents impairment of axon growth and overcompensates microtubule destabilization in cellular models of Alzheimer's disease and related Tau pathologies.Frontiers in medicine · 2025Article
- Amyloid-β oligomers increase the binding and internalization of tau oligomers in human synapses.Acta neuropathologica · 2024Article
- Proteins clump: Mechanics and transport during neurodegeneration.Biophysical journal · 2024Article
- Empowering Naringin's Anti-Inflammatory Effects through Nanoencapsulation.International journal of molecular sciences · 2024Article
- Clathrin mediated endocytosis in Alzheimer's disease: cell type specific involvement in amyloid beta pathology.Frontiers in aging neuroscience · 2024Review
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- ATG5 provides host protection acting as a switch in the atg8ylation cascade between autophagy and secretion.Developmental cell · 2023Article
- Article
- Internalized Amyloid-β (1-42) Peptide Inhibits the Store-Operated Calcium Entry in HT-22 Cells.International journal of molecular sciences · 2022Article
- Novel brain-targeted nanomicelles for anti-glioma therapy mediated by the ApoE-enriched protein corona in vivo.Journal of nanobiotechnology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interactions between amyloid-β peptide (Aβ) and the cell membrane include interaction with membrane lipids and binding to membrane receptors, both of which are considered to be the toxicity mechanisms of Aβ. However, it is unclear whether both mechanisms lead to cytotoxicity. Thus, we aimed to analyze these two mechanisms of Aβ42 interaction with cell membranes under different Aβ aggregation states. To this end, model membrane experiments were conducted. Quantitative analysis of Aβ42 monomers or oligomers bound to the membrane of neuro-2a cells was also performed, and laser confocal microscopy was employed to assess endocytosis of FITC-Aβ42 monomers or oligomers by neuro-2a cells. We found that the binding capacity of Aβ42 to membrane lipids was weak and that the amount of Aβ42 bound to membrane lipids was low. Moreover, clathrin-mediated endocytosis of Aβ42 oligomers by neuro-2a cells was observed. Endocytosis serves as a key mode of interaction between extracellular Aβ42 and neurons. These findings provide insights into the mechanisms underlying Aβ oligomer metabolism.
Indexed as
Identifiers
What OpenQuestion holds
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.