ArticleThe journal of physical chemistry. B2014
Activity and architecture of pyroglutamate-modified amyloid-β (AβpE3-42) pores.
Article in The journal of physical chemistry. B, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Safety, tolerability and efficacy of the glutaminyl cyclase inhibitor PQ912 in Alzheimer's disease: results of a randomized, double-blind, placebo-controlled phase 2a study.Alzheimer's research & therapy · 2018Trial
- Immunomagnetic reduction detects amyloid β 1-42, but neitherRSC advances · 2026Article
- Inhibition of the QPCT-PDIA4 axis rescues ΔF508 and N1303K CFTR in cystic fibrosis.Nature communications · 2026Article
- YIAD-0501 directly dissociates aggregates of full-length and N-terminal pyroglutamate-modified forms of Aβ.Alzheimer's research & therapy · 2026Article
- Pyroglutamylation modulates electronic properties and the conformational ensemble of the amyloid β-peptide.Proteins · 2024Article
- Modulation of Lipid Dynamics in the β-Amyloid Aggregates Induced Membrane Fragmentation.The journal of physical chemistry. B · 2024Article
- Amyloid-β and Phosphorylated Tau are the Key Biomarkers and Predictors of Alzheimer's Disease.Aging and disease · 2024Review
- The structure of tyrosine-10 favors ionic conductance of Alzheimer's disease-associated full-length amyloid-β channels.Nature communications · 2024Article
- Imaging Amyloid-β Membrane Interactions: Ion-Channel Pores and Lipid-Bilayer Permeability in Alzheimer's Disease.Angewandte Chemie (International ed. in English) · 2023Review
- Imaging Amyloid-β Membrane Interactions: Ion-Channel Pores and Lipid-Bilayer Permeability in Alzheimer's Disease.Angewandte Chemie (Weinheim an der Bergstrasse, Germany) · 2023Review
- A MD Simulation Prediction for Regulation ofMolecules (Basel, Switzerland) · 2023Article
- Ion channel formation by N-terminally truncated Aβ (4-42): relevance for the pathogenesis of Alzheimer's disease.Nanomedicine : nanotechnology, biology, and medicine · 2020Article
- Medin Oligomer Membrane Pore Formation: A Potential Mechanism of Vascular Dysfunction.Biophysical journal · 2020Article
- Effector function of anti-pyroglutamate-3 Aβ antibodies affects cognitive benefit, glial activation and amyloid clearance in Alzheimer's-like mice.Alzheimer's research & therapy · 2020Article
- Structure of amyloid βScientific reports · 2019Article
- The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology.EMBO molecular medicine · 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
- Comparative pathobiology of β-amyloid and the unique susceptibility of humans to Alzheimer's disease.Neurobiology of aging · 2016Article
- Immunotherapy targeting pyroglutamate-3 Aβ: prospects and challenges.Molecular neurodegeneration · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Among the family of Aβ peptides, pyroglutamate-modified Aβ (AβpE) peptides are particularly associated with cytotoxicity in Alzheimer's disease (AD). They represent the dominant fraction of Aβ oligomers in the brains of AD patients, but their accumulation in the brains of elderly individuals with normal cognition is significantly lower. Accumulation of AβpE plaques precedes the formation of plaques of full-length Aβ (Aβ1-40/42). Most of these properties appear to be associated with the higher hydrophobicity of AβpE as well as an increased resistance to enzymatic degradation. However, the important question of whether AβpE peptides induce pore activity in lipid membranes and their potential toxicity compared with other Aβ pores is still open. Here we examine the activity of AβpE pores in anionic membranes using planar bilayer electrical recording and provide their structures using molecular dynamics simulations. We find that AβpE pores spontaneously induce ionic current across the membrane and have some similar properties to the other previously studied pores of the Aβ family. However, there are also some significant differences. The onset of AβpE3-42 pore activity is generally delayed compared with Aβ1-42 pores. However, once formed, AβpE3-42 pores produce increased ion permeability of the membrane, as indicated by a greater occurrence of higher conductance electrical events. Structurally, the lactam ring of AβpE peptides induces a change in the conformation of the N-terminal strands of the AβpE3-42 pores. While the N-termini of wild-type Aβ1-42 peptides normally reside in the bulk water region, the N-termini of AβpE3-42 peptides tend to reside in the hydrophobic lipid core. These studies provide a first step to an understanding of the enhanced toxicity attributed to AβpE peptides.
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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.