ArticleJournal of chemical theory and computation2012
All-d-Enantiomer of β-Amyloid Peptide Forms Ion Channels in Lipid Bilayers.
Article in Journal of chemical theory and computation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Kelvin Probe Force Microscopy in Bionanotechnology: Current Advances and Future Perspectives.Advanced materials (Deerfield Beach, Fla.) · 2026Review
- Prediction of Transmembrane Regions, Cholesterol, and Ganglioside Binding Sites in Amyloid-Forming Proteins Indicate Potential for Amyloid Pore Formation.Frontiers in molecular neuroscience · 2021Article
- The on-fibrillation-pathway membrane content leakage and off-fibrillation-pathway lipid mixing induced by 40-residue β-amyloid peptides in biologically relevant model liposomes.Biochimica et biophysica acta. Biomembranes · 2018Article
- Amyloid β Ion Channels in a Membrane Comprising Brain Total Lipid Extracts.ACS chemical neuroscience · 2017Article
- Small molecule NPT-440-1 inhibits ionic flux through AβNanomedicine : nanotechnology, biology, and medicine · 2016Article
- Distinct Membrane Disruption Pathways Are Induced by 40-Residue β-Amyloid Peptides.The Journal of biological chemistry · 2016Article
- The higher level of complexity of K-Ras4B activation at the membrane.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Computational Methods for Structural and Functional Studies of Alzheimer's Amyloid Ion Channels.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Mechanisms of membrane binding of small GTPase K-Ras4B farnesylated hypervariable region.The Journal of biological chemistry · 2015Article
- Differences between amyloid-β aggregation in solution and on the membrane: insights into elucidation of the mechanistic details of Alzheimer's disease.Chemical Society reviews · 2014Review
- Disordered amyloidogenic peptides may insert into the membrane and assemble into common cyclic structural motifs.Chemical Society reviews · 2014Review
- Activity and architecture of pyroglutamate-modified amyloid-β (AβpE3-42) pores.The journal of physical chemistry. B · 2014Article
- Membrane permeation induced by aggregates of human islet amyloid polypeptides.Biophysical journal · 2013Article
- Mechanism of membrane permeation induced by synthetic β-hairpin peptides.Biophysical journal · 2013Article
- Familial Alzheimer's disease Osaka mutant (ΔE22) β-barrels suggest an explanation for the different Aβ1-40/42 preferred conformational states observed by experiment.The journal of physical chemistry. B · 2013Article
- Alzheimer's disease: which type of amyloid-preventing drug agents to employ?Physical chemistry chemical physics : PCCP · 2013Review
- Treadmill exercise prevents learning and memory impairment in Alzheimer's disease-like pathology.Current Alzheimer research · 2013Article
- Mechanisms for the Insertion of Toxic, Fibril-like β-Amyloid Oligomers into the Membrane.Journal of chemical theory and computation · 2013Article
- Amyloid β-protein oligomers and Alzheimer's disease.Alzheimer's research & therapy · 2013Review
- Two-step mechanism of membrane disruption by Aβ through membrane fragmentation and pore formation.Biophysical journal · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common type of senile dementia in aging populations. Amyloid β (Aβ)-mediated dysregulation of ionic homeostasis is the prevailing underlying mechanism leading to synaptic degeneration and neuronal death. Aβ-dependent ionic dysregulation most likely occurs either directly via unregulated ionic transport through the membrane or indirectly via Aβ binding to cell membrane receptors and subsequent opening of existing ion channels or transporters. Receptor binding is expected to involve a high degree of stereospecificity. Here, we investigated whether an Aβ peptide enantiomer, whose entire sequence consists of d-amino acids, can form ion-conducting channels; these channels can directly mediate Aβ effects even in the absence of receptor-peptide interactions. Using complementary approaches of planar lipid bilayer (PLB) electrophysiological recordings and molecular dynamics (MD) simulations, we show that the d-Aβ isomer exhibits ion conductance behavior in the bilayer indistinguishable from that described earlier for the l-Aβ isomer. The d isomer forms channel-like pores with heterogeneous ionic conductance similar to the l-Aβ isomer channels, and the d-isomer channel conductance is blocked by Zn(2+), a known blocker of l-Aβ isomer channels. MD simulations further verify formation of β-barrel-like Aβ channels with d- and l-isomers, illustrating that both d- and l-Aβ barrels can conduct cations. The calculated values of the single-channel conductance are approximately in the range of the experimental values. These findings are in agreement with amyloids forming Ca(2+) leaking, unregulated channels in AD, and suggest that Aβ toxicity is mediated through a receptor-independent, nonstereoselective mechanism.
Identifiers
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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.