ArticleMovement disorders : official journal of the Movement Disorder Society2014
ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.
Article in Movement disorders : official journal of the Movement Disorder Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 45 citations in OpenAlex.
- Deep learning enhanced deciphering of brain activity maps for discovery of therapeutics for brain disorders.iScience · 2025Article
- The Role of α7-Nicotinic Acetylcholine Receptors in the Pathophysiology and Treatment of Parkinson's Disease.International journal of molecular sciences · 2025Review
- Review
- Nicotine-mediated effects in neuronal and mouse models of synucleinopathy.Frontiers in neuroscience · 2023Article
- Levodopa-Induced Dyskinesia in Parkinson's Disease: Pathogenesis and Emerging Treatment Strategies.Cells · 2022Review
- The protective role of cigarette smoking against Parkinson's disease via moderation of the interaction between iron deposition in the nigrostriatal pathway and clinical symptoms.Quantitative imaging in medicine and surgery · 2022Article
- Experimental Models of Cognitive Impairment for Use in Parkinson's Disease Research: The Distance Between Reality and Ideal.Frontiers in aging neuroscience · 2021Review
- Pathophysiological Mechanisms and Experimental Pharmacotherapy for L-Dopa-Induced Dyskinesia.Journal of experimental pharmacology · 2021Review
- Dystonia and levodopa-induced dyskinesias in Parkinson's disease: Is there a connection?Neurobiology of disease · 2019Review
- Thalamic degeneration in MPTP-treated Parkinsonian monkeys: impact upon glutamatergic innervation of striatal cholinergic interneurons.Brain structure & function · 2019Article
- Receptor Ligands as Helping Hands to L-DOPA in the Treatment of Parkinson's Disease.Biomolecules · 2019Review
- Potential Therapeutic Application for Nicotinic Receptor Drugs in Movement Disorders.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2019Review
- The striatal cholinergic system in L-dopa-induced dyskinesias.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- The use of nonhuman primate models to understand processes in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Nicotine from cigarette smoking and diet and Parkinson disease: a review.Translational neurodegeneration · 2017Review
- Optogenetic activation of striatal cholinergic interneurons regulates L-dopa-induced dyskinesias.Neurobiology of disease · 2016Article
- Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson's disease.NPJ Parkinson's disease · 2016Review
- Radiation dosimetry of [(18)F]VAT in nonhuman primates.EJNMMI research · 2015Article
- α7 nicotinic receptor agonists reduce levodopa-induced dyskinesias with severe nigrostriatal damage.Movement disorders : official journal of the Movement Disorder Society · 2015Article
- Preclinical Evidence for a Role of the Nicotinic Cholinergic System in Parkinson's Disease.Neuropsychology review · 2015Review
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Authors and funding
6 authors at 4 institutions in 1 country.
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Abstract
Levodopa-induced dyskinesias (LIDs) are a serious complication of levodopa therapy for Parkinson's disease for which there is little treatment. Accumulating evidence shows that nicotinic acetylcholine receptor (nAChR) drugs decrease LIDs in parkinsonian animals. Here, we examined the effect of two β2 nAChR agonists, ABT-089 and ABT-894, that previously were approved for phase 2 clinical trials for other indications. Two sets of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys were administered levodopa/carbidopa (10 mg/kg and 2.5 mg/kg, respectively) twice daily 5 days a week until they were stably dyskinetic. Each set had a vehicle-treated group, an nAChR agonist-treated group, and a nicotine-treated group as a positive control. Set A monkeys had previously received other nAChR drugs (nAChR drug-primed), whereas Set B monkeys were initially nAChR drug-naive. Both sets were administered the partial agonist ABT-089 (range, 0.01-1.0 mg/kg) orally 5 days a week twice daily 30 minutes before levodopa with each dose given for 1 to 5 weeks. ABT-089 decreased LIDs by 30% to 50% compared with vehicle-treated monkeys. Nicotine reduced LIDs by 70% in a parallel group. After 4 weeks of washout, the effect of the full agonist ABT-894 (range, 0.0001-0.10 mg/kg) was assessed on LIDs in Set A and Set B. ABT-894 reduced LIDs by 70%, similar to nicotine. Both drugs acted equally well at α4β2* and α6β2* nAChRs; however, ABT-089 was 30 to 60 times less potent than ABT-894. Tolerance did not develop for the time periods tested (range, 3-4 months). The nAChR drugs did not worsen parkinsonism or cognitive ability. Emesis, a common problem with nAChR drugs, was not observed. ABT-894 and ABT-089 appear to be good candidate nAChR drugs for the management of LIDs in Parkinson's disease.
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