ReviewMolecular neurobiology2016
The Binding Receptors of Aβ: an Alternative Therapeutic Target for 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 25 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
25 citing papers in PubMed.
- Neuroprotective Activity of 3-((6-(Phenylethynyl)pyridin-3-yl)oxy)quinuclidine: A Potential Ligand for the Treatment of Alzheimer's Disease.ACS chemical neuroscience · 2025Article
- Role of mGluR7 in Alzheimer's disease: pathophysiological insights and therapeutic approaches.Inflammopharmacology · 2025Review
- Evidence that cholinergic mechanisms contribute to hyperexcitability at early stages in Alzheimer's disease.Frontiers in dementia · 2025Review
- Exploring the Benzazoles Derivatives as Pharmacophores for AChE, BACE1, and as Anti-Aβ Aggregation to Find Multitarget Compounds against Alzheimer's Disease.Molecules (Basel, Switzerland) · 2024Review
- Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023Review
- Amyloid precursor protein (APP) and amyloid β (Aβ) interact with cell adhesion molecules: Implications in Alzheimer's disease and normal physiology.Frontiers in cell and developmental biology · 2022Review
- Nicotinic receptor components of amyloid beta 42 proteome regulation in human neural cells.PloS one · 2022Article
- ACU193: An Immunotherapeutic Poised to Test the Amyloid β Oligomer Hypothesis of Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- The transmembrane amyloid precursor C99 protein exhibits non-specific interaction with tau.Biochemical and biophysical research communications · 2021Article
- Mitochondrial Disruption by Amyloid Beta 42 Identified by Proteomics and Pathway Mapping.Cells · 2021Article
- On the Common Journey of Neural Cells through Ischemic Brain Injury and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- HLA in Alzheimer's Disease: Genetic Association and Possible Pathogenic Roles.Neuromolecular medicine · 2020Review
- Amyloid-β Peptide Impact on Synaptic Function and Neuroepigenetic Gene Control Reveal New Therapeutic Strategies for Alzheimer's Disease.Frontiers in molecular neuroscience · 2020Review
- The vexing complexity of the amyloidogenic pathway.Protein science : a publication of the Protein Society · 2019Review
- A Combination of Tri-Leucine and Angiopep-2 Drives a Polyanionic Polymalic Acid Nanodrug Platform Across the Blood-Brain Barrier.ACS nano · 2019Article
- The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia.Frontiers in aging neuroscience · 2019Article
- Proteomic Investigation of Murine Neuronal α7-Nicotinic Acetylcholine Receptor Interacting Proteins.Journal of proteome research · 2018Article
- An acute functional screen identifies an effective antibody targeting amyloid-β oligomers based on calcium imaging.Scientific reports · 2018Article
- Irisin Exerts Neuroprotective Effects on Cultured Neurons by Regulating Astrocytes.Mediators of inflammation · 2018Article
- Allosteric Modulators of the M4 Muscarinic Acetylcholine Receptor.ACS medicinal chemistry letters · 2017Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is one of the most common neurodegenerative disorders, which causes the deterioration of memory and other cognitive abilities of the elderly. Previous lines of research have shown that Aβ is an essential factor in AD pathology and the soluble oligomeric species of Aβ peptide is presumed to be the drivers of synaptic impairment in AD. However, the exact mechanisms underlying Aβ-induced synapse dysfunction are still not fully understood. Recently, increasing evidence suggests that some potential receptors which bind specifically with Aβ may play important roles in inducing the toxicity of the neurons in AD pathology. These receptors include the cellular prion protein (PrPc), the α7 nicotinic acetylcholine receptor (α7nAChR), the p75 neurotrophin receptor (p75(NTR)), the beta-adrenergic receptors (β-ARs), the Eph receptors, the paired immunoglobulin-like receptor B (PirB), the PirB's human ortholog receptor (LilrB2), and the Fcγ receptor II-b (FcγRIIb). This review summarizes the characters of these prominent receptors and how the bindings of them with Aβ inhibit the LTP, decrease the number of dendritic spine, damage the neurons, and so on in AD pathogenesis. Blocking or rescuing these receptors may have significant importance for AD treatments.
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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.