ReviewInternational journal of molecular sciences2021
Cholinergic Modulation of Neuroinflammation: Focus on α7 Nicotinic Receptor.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.
- Pooled it
- Meta-Analysis on Nicotine's Modulation of HIV-Associated Dementia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Pooled it
- Review
- Functional Expression of Nicotinic Receptors on iPSC-Derived Astrocytes and Signalling Disturbances by a Panel of Neonicotinoid Pesticides and Their Metabolites.International journal of molecular sciences · 2026Article
- Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain.Bioelectronic medicine · 2026Review
- The central cholinergic system as a therapeutic target in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Microglial Adaptations to Chronic Nicotine in the Cerebellum: Proteomic Evidence for Neuroimmune Vulnerability.Journal of proteome research · 2026Article
- The basal forebrain-DMN/solv cholinergic projection mediates the attenuation of brain injury after cardiopulmonary resuscitation.World journal of emergency medicine · 2026Article
- The effects of polysaccharides fromHistology and histopathology · 2026Article
- A new framework for nicotinic receptor-targeted therapeutic strategies in psychiatric and neurodegenerative disorders.Frontiers in cellular neuroscience · 2026Article
- Cholinergic regulation of neuroinflammation: linking microglia, immunometabolism, and neuromodulation.Frontiers in immunology · 2026Review
- Biochemical Alterations Related to Vascular Injury in Smokers: Evidence from Nitric Oxide, Malondialdehyde, Nicotinic Acetylcholine Receptors, and Cotinine.Vascular health and risk management · 2026Article
- Common metabolic, environmental, and molecular mechanisms underlying neurodevelopmental and neurodegenerative disorders.Frontiers in neurology · 2026Review
- Neurovascular Signaling at the Gliovascular Interface: From Flow Regulation to Cognitive Energy Coupling.International journal of molecular sciences · 2025Review
- Dexmedetomidine pretreatment improves postsurgical delay in neurocognitive recovery in aged mice by inhibiting hippocampal microglial activation via activation of cholinergic anti-inflammatory pathways.BMC neuroscience · 2025Article
- The Neuroprotective Role of Curcumin: From Molecular Pathways to Clinical Translation-A Narrative Review.Nutrients · 2025Review
- The Functional Topology of Phenylpiperazinium Agonists and Antagonists on the Nicotinic Acetylcholine Receptor Landscape: Pointing the Way for Future Therapeutic Management of Inflammation and Neuropathic Pain.ACS chemical neuroscience · 2025Article
- Stereoisomers of Chiral Methyl-Substituted Symmetric and Asymmetric Aryl Piperazinium Compounds Exhibit Distinct Selectivity for α9 and α7 Nicotinic Acetylcholine Receptors.ACS chemical neuroscience · 2025Article
- Targeting Neuronal Alpha7 Nicotinic Acetylcholine Receptor Upregulation in Age-Related Neurological Disorders.Cellular and molecular neurobiology · 2025Review
- AD16 Modulates Microglial Activation and Polarization to Mitigate Neuroinflammation in Ischemic Stroke Models Through α7nAChR-ERK-STAT3 Signaling.CNS neuroscience & therapeutics · 2025Article
6 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All nervous system pathologies (e.g., neurodegenerative/demyelinating diseases and brain tumours) develop neuroinflammation, a beneficial process during pathological events, aimed at removing damaged cells, toxic agents, and/or pathogens. Unfortunately, excessive inflammation frequently occurs during nervous system disorders, becoming a detrimental event capable of enhancing neurons and myelinating glial cell impairment, rather than improving their survival and activity. Consequently, targeting the neuroinflammation could be relevant for reducing brain injury and rescuing neuronal and glial cell functions. Several studies have highlighted the role of acetylcholine and its receptors in the regulation of central and peripheral inflammation. In particular, α7 nicotinic receptor has been described as one of the main regulators of the "brain cholinergic anti-inflammatory pathway". Its expression in astrocytes and microglial cells and the ability to modulate anti-inflammatory cytokines make this receptor a new interesting therapeutic target for neuroinflammation regulation. In this review, we summarize the distribution and physiological functions of the α7 nicotinic receptor in glial cells (astrocytes and microglia) and its role in the modulation of neuroinflammation. Moreover, we explore how its altered expression and function contribute to the development of different neurological pathologies and exacerbate neuroinflammatory processes.
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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.