ReviewMolecular neurobiology2016
The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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.
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Who cites it
46 citing papers in PubMed.
- Pharmacokinetics and pharmacodynamic effect of crenezumab on plasma and cerebrospinal fluid beta-amyloid in patients with mild-to-moderate Alzheimer's disease.Alzheimer's research & therapy · 2020Trial
- ABBY: A phase 2 randomized trial of crenezumab in mild to moderate Alzheimer disease.Neurology · 2018Trial
- Gut Microbiome Changes in Preclinical Alzheimer's Disease.Nutrients · 2026Review
- tRNA-derived fragments elevated in Alzheimer's disease promote Tau aggregation.bioRxiv : the preprint server for biology · 2026Article
- Advances in nano-TCM for Alzheimer's disease: lipid-based carriers integrated with innovative delivery strategies.Journal of nanobiotechnology · 2026Review
- Amyloid Plaques Ameliorate Memory Deficits and Hippocampal Neuron Loss in an Aβ4-42-Driven Alzheimer's Disease Mouse Model.Molecular neurobiology · 2026Article
- Inflammation in Neuronal Intranuclear Inclusion Disease (NIID): mechanisms, biomarkers, and therapeutic implications.Journal of neuroinflammation · 2025Review
- Platycodin D Attenuates Behavioral Deficits, Amyloid-β Accumulation and Mitochondrial Impairment in AD Models by Inhibiting the cGAS-STING Pathway.Neuromolecular medicine · 2025Article
- Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?International journal of molecular sciences · 2025Review
- Comprehending Alzheimer's Disease: Molecular Mechanisms and Treatment Strategies.Current Alzheimer research · 2025Review
- Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions.Ibrain · 2025Review
- Cordycepin mediates neuroprotection against apoptosis via ERK/CREB signaling activation in AβIbrain · 2025Article
- The shift in the fatty acid composition of the circulating lipidome in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Amyloid β oligomer induces cerebral vasculopathy via pericyte-mediated endothelial dysfunction.Alzheimer's research & therapy · 2024Article
- Synthesis of symmetrical and unsymmetrical tetrahydroxybiphenyls and their evaluation as amyloid-β aggregation inhibitors.Letters in organic chemistry · 2024Article
- Effects of Terahertz Radiation on the Aggregation of Alzheimer's Aβ42 Peptide.International journal of molecular sciences · 2023Article
- Alzheimer's Disease: Treatment Strategies and Their Limitations.International journal of molecular sciences · 2022Review
- Aβ and Tau Interact with Metal Ions, Lipid Membranes and Peptide-Based Amyloid Inhibitors: Are These Common Features Relevant in Alzheimer's Disease?Molecules (Basel, Switzerland) · 2022Review
- Phosphodiesterase 5 inhibitor mirodenafil ameliorates Alzheimer-like pathology and symptoms by multimodal actions.Alzheimer's research & therapy · 2022Article
- Deletion ofScience advances · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by amyloid plaque and neurofibrillary tangles (NFT). With the finding that soluble nonfibrillar Aβ levels actually correlate strongly with the severity of the disease, the initial focus on amyloid plaques shifted to the contemporary concept that AD memory failure is caused by soluble Aβ oligomers. The soluble Aβ are known to be more neurotoxicthan fibrillar Aβ species. In this paper, we summarize the essential role of soluble Aβ oligomers in AD and discuss therapeutic strategies that target soluble Aβ oligomers.
Indexed as
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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.