ReviewJournal of neural transmission (Vienna, Austria : 1996)2013
Some molecular mechanisms of dopaminergic and glutamatergic dysfunctioning in Parkinson's disease.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Pathways and Genetic Determinants of Impulse Control Disorders in Parkinson's Disease.Life (Basel, Switzerland) · 2026Review
- Heterocyclic Derivatives in Parkinson's Therapy: Recent Advances and Prospects.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2026Review
- Performance of Force-Field- and Machine Learning-Based Scoring Functions in Ranking MAO-B Protein-Inhibitor Complexes in Relevance to Developing Parkinson's Therapeutics.International journal of molecular sciences · 2020Article
- Neuroprotection in Parkinson's disease: facts and hopes.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Real life evaluation of safinamide effectiveness in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018Article
- Spotlight on opicapone as an adjunct to levodopa in Parkinson's disease: design, development and potential place in therapy.Drug design, development and therapy · 2017Review
- Sigma-1 receptor deficiency reduces MPTP-induced parkinsonism and death of dopaminergic neurons.Cell death & disease · 2015Article
- Changing the face of kynurenines and neurotoxicity: therapeutic considerations.International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder with a considerable socioeconomic burden. The pathomechanism of PD clearly involves the synergistic interaction of dopaminergic and glutamatergic dysfunctioning, including maladaptive corticostriatal synaptoplasticity. Most of the available treatment options have the aim of restoration of the physiological dopaminergic activity. Currently, the most widely used treatment is L-3,4-dihydroxyphenylalanine (L-DOPA), which leads to the best symptomatic relief in PD. However, the long-term use of L-DOPA results in abnormal involuntary movements in almost all cases, the development of these dyskinetic movements also involving maladaptive corticostriatal synaptoplasticity. Perhaps chronic L-DOPA treatment has neurotoxic effects as well, but it has not yet been proved in clinical studies. Another important group of dopamine replacement therapy (DRT)-related side-effects consists of disinhibitory psychopathologies. Recent studies revealed that genetic polymorphisms affecting certain dopaminergic and glutamatergic receptors serve as independent risk factors for the development of these pathological conditions in PD patients. The available scientific data demonstrate that alterations in the kynurenine pathway of the tryptophan metabolism can be observed in PD and these alterations may contribute to the disease pathogenesis and to the occurrence of DRT-related side-effects. Therapeutic strategies that target the restoration of the kynurenine metabolism could therefore hold promise.
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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.