ArticlePloS one2015
α7 Nicotinic acetylcholine receptor-specific antibody induces inflammation and amyloid β42 accumulation in the mouse brain to impair memory.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
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- Detection and pharmacokinetics of licochalcone A in brains of neuroinflammatory mouse model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Elucidating the role of peripheral monocyte nicotinic acetylcholine receptors and inflammation in cognitive outcomes in older adults.Biogerontology · 2025Article
- The Possible Mechanistic Basis of Individual Susceptibility to Spike Protein Injury.Advances in virology · 2025Review
- An original potentiating mechanism revealed by the cryo-EM structures of the human α7 nicotinic receptor in complex with nanobodies.Nature communications · 2023Article
- Effects of Herbs and Derived Natural Products on Lipopolysaccharide-Induced Toxicity: A Literature Review.Oxidative medicine and cellular longevity · 2023Review
- Nicotinic acetylcholine receptors and learning and memory deficits in Neuroinflammatory diseases.Frontiers in neuroscience · 2023Review
- Immunization with 674-685 fragment of SARS-Cov-2 spike protein induces neuroinflammation and impairs episodic memory of mice.Biochemical and biophysical research communications · 2022Article
- Advances in stem cell therapy in Alzheimer's disease: a comprehensive clinical trial review.Stem cell investigation · 2022Review
- Role of Receptors in Relation to Plaques and Tangles in Alzheimer's Disease Pathology.International journal of molecular sciences · 2021Review
- Neuroinflammation Modulation via α7 Nicotinic Acetylcholine Receptor and Its Chaperone, RIC-3.Molecules (Basel, Switzerland) · 2021Review
- Mesenchymal stem cells as a potential therapeutic tool to cure cognitive impairment caused by neuroinflammation.World journal of stem cells · 2021Review
- nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse.Scientific reports · 2021Article
- Involvement of α7nAChR in the Protective Effects of Genistein Against β-Amyloid-Induced Oxidative Stress in Neurons via a PI3K/Akt/Nrf2 Pathway-Related Mechanism.Cellular and molecular neurobiology · 2021Article
- Changing Functional Signatures of Microglia along the Axis of Brain Aging.International journal of molecular sciences · 2021Review
- Neuroimmune Mechanisms as Novel Treatment Targets for Substance Use Disorders and Associated Comorbidities.Frontiers in neuroscience · 2021Review
- Inhibitory Effects of Raw-ExtractMolecules (Basel, Switzerland) · 2020Article
- Different Effects of Nicotine and N-Stearoyl-ethanolamine on Episodic Memory and Brain Mitochondria of α7 Nicotinic Acetylcholine Receptor Knockout Mice.Biomolecules · 2020Article
- Inflammation has synergistic effect with nicotine in periodontitis by up-regulating the expression of α7 nAChR via phosphorylated GSK-3β.Journal of cellular and molecular medicine · 2020Article
- Farnesyl Transferase Inhibitor Lonafarnib Enhances α7nAChR Expression Through Inhibiting DNA Methylation of CHRNA7 and Increases α7nAChR Membrane Trafficking.Frontiers in pharmacology · 2020Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotinic acetylcholine receptors (nAChRs) expressed in the brain are involved in regulating cognitive functions, as well as inflammatory reactions. Their density is decreased upon Alzheimer disease accompanied by accumulation of β-amyloid (Aβ42), memory deficit and neuroinflammation. Previously we found that α7 nAChR-specific antibody induced pro-inflammatory interleukin-6 production in U373 glioblastoma cells and that such antibodies were present in the blood of humans. We raised a hypothesis that α7 nAChR-specific antibody can cause neuroinflammation when penetrating the brain. To test this, C57Bl/6 mice were either immunized with extracellular domain of α7 nAChR subunit α7(1-208) or injected with bacterial lipopolysaccharide (LPS) for 5 months. We studied their behavior and the presence of α3, α4, α7, β2 and β4 nAChR subunits, Aβ40 and Aβ42 and activated astrocytes in the brain by sandwich ELISA and confocal microscopy. It was found that either LPS injections or immunizations with α7(1-208) resulted in region-specific decrease of α7 and α4β2 and increase of α3β4 nAChRs, accumulation of Aβ42 and activated astrocytes in the brain of mice and worsening of their episodic memory. Intravenously transferred α7 nAChR-specific-antibodies penetrated the brain parenchyma of mice pre-injected with LPS. Our data demonstrate that (1) neuroinflammation is sufficient to provoke the decrease of α7 and α4β2 nAChRs, Aβ42 accumulation and memory impairment in mice and (2) α7(1-208) nAChR-specific antibodies can cause inflammation within the brain resulting in the symptoms typical for Alzheimer disease.
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