ReviewCold Spring Harbor perspectives in medicine2016
The Prion-Like Properties of Amyloid-β Assemblies: Implications for Alzheimer's Disease.
Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Exploring the Etiological Links behind Neurodegenerative Diseases: Inflammatory Cytokines and Bioactive Kynurenines.International journal of molecular sciences · 2020Pooled it
- The amino acid substitutions A30W, K28A, and M35C alter amyloid-β peptide toxicity in cell culture and in anFrontiers in aging neuroscience · 2026Article
- Isolated atrial amyloidosis from atrial natriuretic peptide - a common but overlooked cardiac condition.Upsala journal of medical sciences · 2026Review
- The structure of complexes between zinc(ii) cations and histidine-rich repeats from the unstructured N-terminal domain of human prion protein.RSC advances · 2025Review
- Clinical and MRI Correlates of β-Amyloid Load Inconsistent With Its Presumed Neurotoxicity in Cognitively Healthy Ageing.Journal of neurochemistry · 2025Article
- Implications of Mucin-TypeMolecules (Basel, Switzerland) · 2025Review
- Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Evidence Suggesting That Alzheimer's Disease May Be a Transmissible Disorder.International journal of molecular sciences · 2025Article
- The dynamics of prion spreading is governed by the interplay between the non-linearities of tissue response and replication kinetics.iScience · 2024Article
- Microglial senescence in neurodegeneration: Insights, implications, and therapeutic opportunities.Neuroprotection (Chichester, England) · 2024Article
- Evaluating the inter-species transmission risk of amyloid beta peptide aggregates via ingestion.Alzheimer's research & therapy · 2024Article
- Transmission of amyloid-β pathology in humans: a perspective on clinical evidence.Neural regeneration research · 2024Article
- Secondary Modification of S100B Influences Anti Amyloid-β Aggregation Activity and Alzheimer's Disease Pathology.International journal of molecular sciences · 2024Article
- Hippocampal injections of soluble amyloid-beta oligomers alter electroencephalographic activity during wake and slow-wave sleep in rats.Alzheimer's research & therapy · 2023Article
- Overview of the Special Issue "Protein-Based Infection, Inheritance, and Memory".International journal of molecular sciences · 2023Article
- Review
- Ganglioside GM1 produces stable, short, and cytotoxic AβChemical communications (Cambridge, England) · 2023Article
- Article
- Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.PLoS pathogens · 2022Article
- Modeling the Competition between Misfolded Aβ Conformers That Produce Distinct Types of Amyloid Pathology in Alzheimer's Disease.Biomolecules · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Since the discovery that prion diseases can be transmitted to experimental animals by inoculation with afflicted brain matter, researchers have speculated that the brains of patients suffering from other neurodegenerative diseases might also harbor causative agents with transmissible properties. Foremost among these disorders is Alzheimer's disease (AD), the most common cause of dementia in the elderly. A growing body of research supports the concept that the pathogenesis of AD is initiated and sustained by the endogenous, seeded misfolding and aggregation of the protein fragment amyloid-β (Aβ). At the molecular level, this mechanism of nucleated protein self-assembly is virtually identical to that of prions consisting of the prion protein (PrP). The formation, propagation, and spread of Aβ seeds within the brain can thus be considered a fundamental feature of AD pathogenesis.
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.