ReviewBiochemical pharmacology2015
Alpha7 nicotinic receptors as therapeutic targets for Parkinson's disease.
Review in Biochemical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 119 citations in OpenAlex.
- PARP1 suppression by α7 nAChR activation attenuated α-synuclein-induced neurotoxicity in Parkinson's disease.Protein & cell · 2026Article
- Deep learning-driven discovery and mechanism of action study of a minimalist conopeptide targetingActa pharmaceutica Sinica. B · 2026Article
- Dynamic Smoking Patterns and Risk of Parkinson Disease and All-Cause Mortality: A Competing Risk Analysis Approach.Neurology · 2026Article
- Neuroimmune interactions in inflammatory bowel disease: Role of intestinal macrophages and the cholinergic pathway.World journal of gastroenterology · 2025Review
- A Narrative Review on the Role of Microbiota and Microglia in Premotor Symptoms of Parkinson's Disease.Neurotoxicity research · 2025Review
- Effects of Swapping 5HT3 and α7 Residues in Chimeric Receptor Proteins on RIC3 and NACHO Chaperone Actions.Molecules (Basel, Switzerland) · 2025Article
- Targeting Neuronal Alpha7 Nicotinic Acetylcholine Receptor Upregulation in Age-Related Neurological Disorders.Cellular and molecular neurobiology · 2025Review
- Selective Inhibition of Rat α7 Nicotinic Acetylcholine Receptors by LvID, a Newly Characterized α4/7-Conotoxin fromJournal of medicinal chemistry · 2025Article
- Structural basis for allosteric agonism of human α7 nicotinic acetylcholine receptors.Cell discovery · 2025Article
- The Role of α7-Nicotinic Acetylcholine Receptors in the Pathophysiology and Treatment of Parkinson's Disease.International journal of molecular sciences · 2025Review
- Transcutaneous Auricular Vagus Stimulation Attenuates LPS-Induced Depression-Like Behavior by Regulating Central α7nAChR/JAK2 Signaling.Molecular neurobiology · 2025Article
- A comprehensive review of natural compounds and their structure-activity relationship in Parkinson's disease: exploring potential mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hidden complexity of α7 nicotinic acetylcholine receptor desensitization revealed by MD simulations and Markov state modeling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting the cholinergic anti-inflammatory pathway: an innovative strategy for treating diseases.Molecular biology reports · 2025Review
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Role of the Central Cholinergic Nervous System in Motor and Non-Motor Symptoms of Parkinson's Disease.Current neuropharmacology · 2025Review
- Potential Protective Effects of Pungent Flavor Components in Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2024Review
- Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson's Disease.Cells · 2024Review
- Article
- Unprecedented effect of vitamin D3 on T-cell receptor beta subunit and alpha7 nicotinic acetylcholine receptor expression in a 3-nitropropionic acid induced mouse model of Huntington's disease.IBRO neuroscience reports · 2023Article
2 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 1 institution in 1 country.
Funding
Abstract
Accumulating evidence suggests that CNS α7 nicotinic acetylcholine receptors (nAChRs) are important targets for the development of therapeutic approaches for Parkinson's disease. This progressive neurodegenerative disorder is characterized by debilitating motor deficits, as well as autonomic problems, cognitive declines, changes in affect and sleep disturbances. Currently l-dopa is the gold standard treatment for Parkinson's disease motor problems, particularly in the early disease stages. However, it does not improve the other symptoms, nor does it reduce the inevitable disease progression. Novel therapeutic strategies for Parkinson's disease are therefore critical. Extensive pre-clinical work using a wide variety of experimental models shows that nicotine and nAChR agonists protect against damage to nigrostriatal and other neuronal cells. This observation suggests that nicotine and/or nAChR agonists may be useful as disease modifying agents. Additionally, studies in several parkinsonian animal models including nonhuman primates show that nicotine reduces l-dopa-induced dyskinesias, a side effect of l-dopa therapy that may be as incapacitating as Parkinson's disease itself. Work with subtype selective nAChR agonists indicate that α7 nAChRs are involved in mediating both the neuroprotective and antidyskinetic effects, thus offering a targeted strategy with optimal beneficial effects and minimal adverse responses. Here, we review studies demonstrating a role for α7 nAChRs in protection against neurodegenerative effects and for the reduction of l-dopa-induced dyskinesias. Altogether, this work suggests that α7 nAChRs may be useful targets for reducing Parkinson's disease progression and for the management of the dyskinesias that arise with l-dopa therapy.
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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.