ReviewInternational journal of molecular sciences2018
Cellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer's Disease.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
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.
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
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.
- A Systematic Review on the Effects of Different Types of Probiotics in Animal Alzheimer's Disease Studies.Frontiers in psychiatry · 2022Pooled it
- The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer's Disease (AD).International journal of molecular sciences · 2019Pooled it
- Exposure to oligomeric and fibrillar species of amyloid-β induces toxicity and impairs extravillous trophoblast cell function in vitro.Placenta · 2026Article
- Article
- Advances in nano-TCM for Alzheimer's disease: lipid-based carriers integrated with innovative delivery strategies.Journal of nanobiotechnology · 2026Review
- Low Brain Levels of Dietary Polyphenols and Their Conjugates: Reassessing Mechanisms of Alzheimer's Disease Prevention.Journal of dementia and alzheimer's disease · 2026Article
- Tau Protein Aggregation Inhibitors-Therapeutic Strategy for Concurrent Tau and Amyloid Aggregation Inhibition.Biomedicines · 2026Review
- Neurotrophic and Neurotoxic Effects of Aβ42 and Its Oligomers on Neuronal Survival: Revealed by Their Opposite Influence on the Potency of Extracellular BDNF.International journal of molecular sciences · 2025Article
- Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis.Neurochemical research · 2025Review
- Master regulators of neurogenesis: the dynamic roles of Ephrin receptors across diverse cellular niches.Translational psychiatry · 2024Review
- Review
- The Role of α-Synuclein in Etiology of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Preparation and Characterization of Zn(II)-Stabilized AβACS chemical neuroscience · 2024Article
- Amyloid-β and Phosphorylated Tau are the Key Biomarkers and Predictors of Alzheimer's Disease.Aging and disease · 2024Review
- Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases.Molecular neurodegeneration · 2024Review
- Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer's disease.Acta neuropathologica · 2024Article
- A Combinational Therapy for Preventing and Delaying the Onset of Alzheimer's Disease: A Focus on Probiotic and Vitamin Co-Supplementation.Antioxidants (Basel, Switzerland) · 2024Review
- The Complex Interplay between Toxic Hallmark Proteins, Calmodulin-Binding Proteins, Ion Channels, and Receptors Involved in Calcium Dyshomeostasis in Neurodegeneration.Biomolecules · 2024Review
- Post-translational modifications of beta-amyloid alter its transport in the blood-brain barrierFrontiers in molecular neuroscience · 2024Article
- Switching On/Off Amyloid Plaque Formation in Transgenic Animal Models of Alzheimer's Disease.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is estimated that Alzheimer’s disease (AD) affects tens of millions of people, comprising not only suffering patients, but also their relatives and caregivers. AD is one of age-related neurodegenerative diseases (NDs) characterized by progressive synaptic damage and neuronal loss, which result in gradual cognitive impairment leading to dementia. The cause of AD remains still unresolved, despite being studied for more than a century. The hallmark pathological features of this disease are senile plaques within patients’ brain composed of amyloid beta (Aβ) and neurofibrillary tangles (NFTs) of Tau protein. However, the roles of Aβ and Tau in AD pathology are being questioned and other causes of AD are postulated. One of the most interesting theories proposed is the causative role of amyloid β oligomers (AβOs) aggregation in the pathogenesis of AD. Moreover, binding of AβOs to cell membranes is probably mediated by certain proteins on the neuronal cell surface acting as AβO receptors. The aim of our paper is to describe alternative hypotheses of AD etiology, including genetic alterations and the role of misfolded proteins, especially Aβ oligomers, in Alzheimer’s disease. Furthermore, in this review we present various putative cellular AβO receptors related to toxic activity of oligomers.
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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.