Emerging drugs for the treatment of L-DOPA-induced dyskinesia: an update

Alshimemeri, Sohaila; Fox, Susan H.; Visanji, Naomi P.

doi:10.1080/14728214.2020.1763954

Cited by 13 publications

(8 citation statements)

References 145 publications

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“…NMDA receptor channel blocker memantine was approved as a therapeutic for Alzheimer's disease in 2003, and the channel blocker esketamine has been approved for treatment-resistant depression (Supplemental Table 12). Amantadine is commonly prescribed for L-DOPA-induced dyskinesias in Parkinson disease (AlShimemeri et al, 2020) and generally considered a low-affinity NMDA receptor channel blocker (Section VII. Pharmacology of Orthosteric Ligands and Channel Blockers) (Supplemental Table 12).…”

Section: A Overview Of Focus Areas In Drug Discoverymentioning

confidence: 99%

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Hansen¹,

Wollmuth²,

Bowie³

et al. 2021

Pharmacol Rev

332

445

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Section: A Overview Of Focus Areas In Drug Discoverymentioning

confidence: 99%

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Hansen¹,

Wollmuth²,

Bowie³

et al. 2021

Pharmacol Rev

332

445

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“…This could be explained by the fact that these respective AE occur at different stages of the disease-very early or rather late, respectively. Thus, HTR1A agonists could be used to prevent or treat these adverse events as well [8,51,52]. Additionally, the genetic variants pointed out could also serve as predictive biomarkers of the analysed AE and help guide the treatment of PD patients.…”

Section: Discussionmentioning

confidence: 99%

Serotonin-Related Functional Genetic Variants Affect the Occurrence of Psychiatric and Motor Adverse Events of Dopaminergic Treatment in Parkinson’s Disease: A Retrospective Cohort Study

Redenšek

Blagus

Trošt

et al. 2022

JPM

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The serotonergic system is important in Parkinson’s disease (PD) pathogenesis as it can take over dopamine production after a large portion of dopaminergic neurons is lost through neurodegeneration. The aim of this study was to evaluate the effect of genetic variability of serotonergic genes on the occurrence of motor complications and psychiatric adverse events (AE) due to dopaminergic treatment. We enrolled 231 patients and their clinical data were collected. Genotyping was performed for eight genetic variants. Logistic regression was used for analysis. Carriers of the HTR1A rs6295 GC genotype (OR = 2.58; 95% CI = 1.15–5.78; p = 0.021), TPH2 rs4290270 AA genotype (OR = 2.78; 95% CI = 1.08–7.03; p = 0.034), and at least one TPH2 rs4570625 T allele (OR = 1.86; 95% CI = 1.00–3.44; p = 0.047) had increased risk for visual hallucinations (VH). Additionally, carriers of at least one SLC6A4 5-HTTPLR rs25531 S (OR = 0.52; 95% CI = 0.28–0.96; p = 0.037) or at least one LG allele (OR = 0.37; 95% CI = 0.14–0.97; p = 0.044) had a decreased chance for VH. Constructed haplotypes of the TPH2 showed increased risk for VH (OR = 1.94; 95% CI = 1.06–3.55; p = 0.032) and impulse control disorders (OR = 5.20; 95% CI = 1.86–14.50; p = 0.002). Finally, individual gene–gene interactions showed decreased odds for the development of motor AE. Our findings suggest that the serotonergic pathway may play an important role in the development of AE resulting from dopaminergic treatment.

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“…PD is a multifactorial disease caused both by genetic modification and different environmental factors [6]. Moreover, PD is a disorder characterized by a combination of motor symptoms (including tremor, rigidity, gait abnormality, and bradykinesia) and non-motor symptoms [7].…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation and Dyskinesia: A Possible Causative Relationship?

Cardinale,

de Iure,

Picconi

2024

Brain Sciences

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Levodopa (L-DOPA) treatment represents the gold standard therapy for Parkinson’s disease (PD) patients. L-DOPA therapy shows many side effects, among them, L-DOPA-induced dyskinesias (LIDs) remain the most problematic. Several are the mechanisms underlying these processes: abnormal corticostriatal neurotransmission, pre- and post-synaptic neuronal events, changes in gene expression, and altered plasticity. In recent years, researchers have also suggested non-neuronal mechanisms as a possible cause for LIDs. We reviewed recent clinical and pre-clinical studies on neuroinflammation contribution to LIDs. Microglia and astrocytes seem to play a strategic role in LIDs phenomenon. In particular, their inflammatory response affects neuron-glia communication, synaptic activity and neuroplasticity, contributing to LIDs development. Finally, we describe possible new therapeutic interventions for dyskinesia prevention targeting glia cells.

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Emerging drugs for the treatment of L-DOPA-induced dyskinesia: an update

Cited by 13 publications

References 145 publications

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels

Serotonin-Related Functional Genetic Variants Affect the Occurrence of Psychiatric and Motor Adverse Events of Dopaminergic Treatment in Parkinson’s Disease: A Retrospective Cohort Study

Neuroinflammation and Dyskinesia: A Possible Causative Relationship?

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