ReviewChemical science2023
The supersaturation perspective on the amyloid hypothesis.
Review in Chemical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 16 citations in OpenAlex.
- Accelerated amyloid fibril formation at the interface of liquid-liquid phase-separated droplets by depletion interactions.Protein science : a publication of the Protein Society · 2025Article
- Reduced protein solubility - cause or consequence in amyloid disease?QRB discovery · 2025Review
- From Plaques to Pathways in Alzheimer's Disease: The Mitochondrial-Neurovascular-Metabolic Hypothesis.International journal of molecular sciences · 2024Review
- Cavity Lasing of Thioflavin T in the Condensed Phase for Discrimination between Surface Interaction and β-Sheet Groove Binding in Alzheimer-Linked Peptides.The journal of physical chemistry letters · 2024Article
- Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms.BMB reports · 2024Review
- EPR Studies of Aβ42 Oligomers Indicate a Parallel In-Register β-Sheet Structure.ACS chemical neuroscience · 2024Article
- The effect of human PBMCs immobilization on their Аβ42 aggregates-dependent proinflammatory state on a cellular model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Development of therapeutic interventions for Alzheimer's over the past three decades has been guided by the amyloid hypothesis, which puts Aβ deposition as the initiating event of a pathogenic cascade leading to dementia. In the current form, the amyloid hypothesis lacks a comprehensive framework that considers the complex nature of Aβ aggregation. The explanation of how Aβ deposition leads to downstream pathology, and how reducing Aβ plaque load
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.