ReviewAlzheimer's research & therapy2013
On the subject of rigor in the study of amyloid β-protein assembly.
Review in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed.
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- NLRP3 inflammasome in neurodegenerative disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Assessing Reproducibility in Amyloid β Research: Impact of Aβ Sources on Experimental Outcomes.Chembiochem : a European journal of chemical biology · 2020Article
- Rhodamine-Based Metal Chelator: A Potent Inhibitor of Metal-Catalyzed Amyloid Toxicity.ACS omega · 2020Article
- Real-Time BODIPY-Binding Assay To Screen Inhibitors of the Early Oligomerization Process of Aβ1-42 Peptide.Chembiochem : a European journal of chemical biology · 2020Article
- A DFT-Assisted Topological Analysis of Four Polymorphic, S-Shaped Aβ42 Fibril Structures.Chembiochem : a European journal of chemical biology · 2019Article
- A novel crosslinking protocol stabilizes amyloid β oligomers capable of inducing Alzheimer's-associated pathologies.Journal of neurochemistry · 2019Article
- A Human Embryonic Stem Cell Model of Aβ-Dependent Chronic Progressive Neurodegeneration.Frontiers in neuroscience · 2019Article
- Questions concerning the role of amyloid-β in the definition, aetiology and diagnosis of Alzheimer's disease.Acta neuropathologica · 2018Review
- The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade.Journal of Alzheimer's disease : JAD · 2018Review
- Using chirality to probe the conformational dynamics and assembly of intrinsically disordered amyloid proteins.Scientific reports · 2017Article
- A human scFv antibody that targets and neutralizes high molecular weight pathogenic amyloid-β oligomers.Journal of neurochemistry · 2017Article
- 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose Binds to the N-terminal Metal Binding Region to Inhibit AmyloidInternational journal of mass spectrometry · 2017Article
- Retinal amyloid pathology and proof-of-concept imaging trial in Alzheimer's disease.JCI insight · 2017Article
- Preparation of pure populations of covalently stabilized amyloid β-protein oligomers of specific sizes.Analytical biochemistry · 2017Article
- Pittsburgh Compound-B (PiB) binds amyloid β-protein protofibrils.Journal of neurochemistry · 2017Article
- Assembly of Peptides Derived from β-Sheet Regions of β-Amyloid.Journal of the American Chemical Society · 2016Article
- Mechanism of C-Terminal Fragments of Amyloid β-Protein as Aβ Inhibitors: Do C-Terminal Interactions Play a Key Role in Their Inhibitory Activity?The journal of physical chemistry. B · 2016Article
- Amyloid β-Protein Assembly and Alzheimer's Disease: Dodecamers of Aβ42, but Not of Aβ40, Seed Fibril Formation.Journal of the American Chemical Society · 2016Article
- Role of Species-Specific Primary Structure Differences in Aβ42 Assembly and Neurotoxicity.ACS chemical neuroscience · 2015Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to Thomas Kuhn, the success of 'normal science,' the science we all practice on a daily basis, depends on the adherence to, and practice of, a paradigm accepted by the scientific community. When great scientific upheavals occur, they involve the rejection of the current paradigm in favor of a new paradigm that better integrates the facts available and better predicts the behavior of a particular scientific system. In the field of Alzheimer's disease, a recent example of such a paradigm shift has been the apparent rejection of the 'amyloid cascade hypothesis,' promulgated by Hardy and Higgins in 1992 to explain the etiology of Alzheimer's disease, in favor of what has been referred to as the 'oligomer cascade hypothesis'. This paradigm shift has been breathtaking in its rapidity, its pervasiveness in the Alzheimer's disease field, and its adoption in an increasing number of other fields, including those of Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and the prionoses. However, these facts do not mean, a priori, that the experiments extant, and any re-interpretation of them, should be accepted by rote as support for the new paradigm. In the discussion that follows, I consider the foundational studies leading to the oligomer cascade hypothesis and evaluate the current state of the paradigm. I argue here that, more often than not, insufficient rigor has been applied in studies upon which this new paradigm has been based. Confusion, rather than clarity, has resulted. If the field is to make progress forward using as its paradigmatic basis amyloid β-protein oligomerization, then an epistemological re-evaluation of the amyloid β-protein oligomer system is required.
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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.