ArticleThe Journal of biological chemistry2012
Molecular plasticity regulates oligomerization and cytotoxicity of the multipeptide-length amyloid-β peptide pool.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed.
- The effect of LCZ696 (sacubitril/valsartan) on amyloid-β concentrations in cerebrospinal fluid in healthy subjects.British journal of clinical pharmacology · 2016Trial
- BACE-1 and ADAM-10 as Potential Peripheral Biomarkers for Alzheimer's Disease.Current pharmaceutical design · 2026Review
- Amyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity.Molecular neurodegeneration · 2023Article
- Heterotypic Amyloid β interactions facilitate amyloid assembly and modify amyloid structure.The EMBO journal · 2022Article
- Dynamic observations of various oligomers in amyloidBiochemistry and biophysics reports · 2022Article
- Effects of Aβ-derived peptide fragments on fibrillogenesis of Aβ.Scientific reports · 2021Article
- α-CGRP disrupts amylin fibrillization and regulates insulin secretion: implications on diabetes and migraine.Chemical science · 2021Article
- The Aβ(1-38) peptide is a negative regulator of the Aβ(1-42) peptide implicated in Alzheimer disease progression.Scientific reports · 2021Article
- Single Point Mutation from E22-to-K in AOxidative medicine and cellular longevity · 2020Article
- Female Sex Hormones and Cardiac Pressure Overload Independently Contribute to the Cardiogenic Dementia Profile in Yucatan Miniature Swine.Frontiers in cardiovascular medicine · 2019Article
- Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP.Brain : a journal of neurology · 2018Article
- Energetics Underlying Twist Polymorphisms in Amyloid Fibrils.The journal of physical chemistry. B · 2018Article
- Amyloid β-peptides 1-40 and 1-42 form oligomers with mixed β-sheets.Chemical science · 2017Article
- Cerebrospinal Fluid Levels of Amyloid Beta 1-43 Mirror 1-42 in Relation to Imaging Biomarkers of Alzheimer's Disease.Frontiers in aging neuroscience · 2017Article
- C-Terminal Threonine Reduces Aβ43 Amyloidogenicity Compared with Aβ42.Journal of molecular biology · 2016Article
- Isotope-edited FTIR reveals distinct aggregation and structural behaviors of unmodified and pyroglutamylated amyloid β peptides.Physical chemistry chemical physics : PCCP · 2015Article
- Two distinct β-sheet structures in Italian-mutant amyloid-beta fibrils: a potential link to different clinical phenotypes.Cellular and molecular life sciences : CMLS · 2015Article
- Article
- Self-Assembly of Aβ40, Aβ42 and Aβ43 Peptides in Aqueous Mixtures of Fluorinated Alcohols.PloS one · 2015Article
- Chatting with the neighbors: crosstalk between Rho-kinase (ROCK) and other signaling pathways for treatment of neurological disorders.Frontiers in neuroscience · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current therapeutic approaches under development for Alzheimer disease, including γ-secretase modulating therapy, aim at increasing the production of Aβ(1-38) and Aβ(1-40) at the cost of longer Aβ peptides. Here, we consider the aggregation of Aβ(1-38) and Aβ(1-43) in addition to Aβ(1-40) and Aβ(1-42), in particular their behavior in mixtures representing the complex in vivo Aβ pool. We demonstrate that Aβ(1-38) and Aβ(1-43) aggregate similar to Aβ(1-40) and Aβ(1-42), respectively, but display a variation in the kinetics of assembly and toxicity due to differences in short timescale conformational plasticity. In biologically relevant mixtures of Aβ, Aβ(1-38) and Aβ(1-43) significantly affect the behaviors of Aβ(1-40) and Aβ(1-42). The short timescale conformational flexibility of Aβ(1-38) is suggested to be responsible for enhancing toxicity of Aβ(1-40) while exerting a cyto-protective effect on Aβ(1-42). Our results indicate that the complex in vivo Aβ peptide array and variations thereof is critical in Alzheimer disease, which can influence the selection of current and new therapeutic strategies.
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.