ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Dissociating beta-amyloid from alpha 7 nicotinic acetylcholine receptor by a novel therapeutic agent, S 24795, normalizes alpha 7 nicotinic acetylcholine and NMDA receptor function in Alzheimer's disease brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 48 papers.
What it found
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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
48 citing papers in PubMed, 101 citations in OpenAlex.
- A randomized, placebo-controlled study investigating the nicotinic α7 agonist, RG3487, for cognitive deficits in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Trial
- Repetitive transcranial magnetic stimulation enhances BDNF-TrkB signaling in both brain and lymphocyte.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Trial
- Docking Analysis of Drugs Used in the Treatment of Alzheimer's Disease, Using Cell Membrane Receptors and Enzymes of the Kynurenine Pathway: A Pilot Study.International journal of molecular sciences · 2026Article
- The microcirculation, the blood-brain barrier, and the neurovascular unit in health and Alzheimer disease: The aberrant pericyte is a central player.Pharmacological reviews · 2025Review
- Review
- The duality of amyloid-β: its role in normal and Alzheimer's disease states.Molecular brain · 2024Review
- Neuroprotective Effect ofBiology · 2024Article
- Neuroprotective Effect of Quercetin and Memantine against AlClMolecules (Basel, Switzerland) · 2023Article
- Positron Emission Tomography in Animal Models of Alzheimer's Disease Amyloidosis: Translational Implications.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Postnatal Cytoarchitecture and Neurochemical Hippocampal Dysfunction in Down Syndrome.Journal of clinical medicine · 2021Article
- Receptor-Dependent and Independent Regulation of Voltage-Gated CaInternational journal of molecular sciences · 2021Review
- The Cholinergic System, the Adrenergic System and the Neuropathology of Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Multi-Target Effects of the Cannabinoid CP55940 on Familial Alzheimer's Disease PSEN1 E280A Cholinergic-Like Neurons: Role of CB1 Receptor.Journal of Alzheimer's disease : JAD · 2021Article
- Amyloid Beta Peptide (AβJournal of clinical medicine · 2020Article
- Crosstalk between the MCellular signalling · 2020Review
- Evidence that Brain-Reactive Autoantibodies Contribute to Chronic Neuronal Internalization of Exogenous Amyloid-β1-42 and Key Cell Surface Proteins During Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2020Article
- Insulin and adipokine signaling and their cross-regulation in postmortem human brain.Neurobiology of aging · 2019Article
- Nicotinic Acetylcholine Receptor Agonists for the Treatment of Alzheimer's Dementia: An Update.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2019Review
- Alzheimer's Disease as a Membrane Disorder: Spatial Cross-Talk Among Beta-Amyloid Peptides, Nicotinic Acetylcholine Receptors and Lipid Rafts.Frontiers in cellular neuroscience · 2019Review
- BACE1 Function and Inhibition: Implications of Intervention in the Amyloid Pathway of Alzheimer's Disease Pathology.Molecules (Basel, Switzerland) · 2017Review
Corrections and comments
- Expression of concern · 2021-12-17Concerns/Issues about Image · · see also: https://pubpeer.com/publications/F30562EB414EB792A9474E55318F0B
- Expression of concern
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by synaptic dysfunction and cardinal neuropathological features including amyloid plaques and neurofibrillary tangles. Soluble amyloid-beta (Abeta) can suppress synaptic activities by interacting with alpha7 nicotinic acetylcholine receptors (alpha7nAChRs). Here, we show that alpha7nAChR and NMDA glutamatergic receptor (NMDAR) activities are severely compromised in synaptosomes prepared from AD and Abeta(1-42) (Abeta42)-exposed control frontal cortex slices from postmortem tissue. Whereas Abeta(12-28) prevents Abeta42 from binding to alpha7nAChRs, 2-[2-(4-bromophenyl)-2-oxoethyl]-1-methyl pyridinium (S 24795), a novel alpha7nAChR partial agonist, facilitates release of Abeta42 from Abeta42-alpha7nAChR and -Abeta42 complexes. S 24795 interacts with alpha7nAChR and Abeta(15-20) region of the Abeta42 to enable partial recovery of the alpha7nAChR and NMDAR channel function. These findings suggest that the Abeta-alpha7nAChR interaction may be an upstream pathogenic event in AD and demonstrate that some recovery of neuronal channel activities may be achieved in AD brains by removing Abeta from alpha7nAChRs.
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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.