Drug screening revealed that 2-aminoethoxydiphenyl borate (2-ABP), nifedipine, nimodipine, flunarizine and ethoxzolamide significantly decreased abnormal movements in unc-77(e625) animals.
Six MPTP-lesioned marmosets with stable dyskinesia and PLBs were administered EMD-281,014 (0.1, 1 and 10 mg/kg) or vehicle in combination with L-DOPA and the effect on dyskinesia, PLBs and parkinsonism was assessed.
Inhibition of miR-543-3p can rescue the expression and function of GLT-1 and relieve dyskinesia in the PD model, which suggests that inhibition of miR-543-3p could serve as a potential therapeutic target for PD.
Nicotinic cholinergic drugs, including nicotine and selective nAChR receptor agonists, reduce L-dopa-induced dyskinesias, as well as antipsychotic-induced tardive dyskinesia, and may be useful in Tourette's syndrome and ataxia.
These data suggest that decreasing tumor necrosis factor-α levels may be useful to reduce the appearance of dyskinesia, and thalidomide, and more potent derivatives may provide an effective therapeutic approach to dyskinesia.
The "NR2B/NMDAR-nNOS/NO-SNO-Src-p-Src-NR2B/NMDAR" signaling cycle may be the molecular basis of NR2B tyrosine phosphorylation upward positive feedback, which demonstrates the possibility as one latent target for dyskinesia therapy.
The "NR2B/NMDAR-nNOS/NO-SNO-Src-p-Src-NR2B/NMDAR" signaling cycle may be the molecular basis of NR2B tyrosine phosphorylation upward positive feedback, which demonstrates the possibility as one latent target for dyskinesia therapy.
Acupuncture combined with the administration of MCH receptor antagonist did not have any beneficial effects on dyskinesia in L-DOPA-injected ak/ak mice, but the intranasal administration of MCH attenuated LID to the same degree as acupuncture in both ak/ak and 6-OHDA mice with LID.
Augmented function of N-methyl-d-aspartate receptor subunit 2B (NR2B) and Src protein tyrosine kinase have been demonstrated to get involved in the pathological mechanisms of dyskinesia.
We found that LBPM developed less AIM severity compared with standard L-dopa administration, whereas selective deletion of β-arrestin2 in striatum neurons dramatically enhanced the severity of dyskinesia by LBPM.
While repeated administration induced a partial desensitization of the fosB gene in the striatum, it did not suppress its activity completely, which could explain why dyskinesia appears after chronic levodopa treatment.
Modulation of presynaptic metabotropic glutamate receptor 4 (mGlu<sub>4</sub>) by an allosteric ligand has been proposed as a promising therapeutic target in Parkinson's disease and levodopa-induced dyskinesia.
The "NR2B/NMDAR-nNOS/NO-SNO-Src-p-Src-NR2B/NMDAR" signaling cycle may be the molecular basis of NR2B tyrosine phosphorylation upward positive feedback, which demonstrates the possibility as one latent target for dyskinesia therapy.
Some specific phenomenology of movement disorders are likely to give clue about the type of antibody, for instance, presence of paroxysmal dystonia (facio-brachial dystonic seizures) are a pointer toward presence of LGI-1 antibodies, and orofacial lingual dyskinesia is associated with NMDAR associated encephalitis.
Therefore, our findings demonstrate that ALDH1A1-synthesized RA is required for postsynaptic MOR1 expression in the postnatal and adult dorsal striatum, supporting potential therapeutic benefits of RA supplementation in moderating L-DOPA-induced dyskinesia.
We found that LBPM developed less AIM severity compared with standard L-dopa administration, whereas selective deletion of β-arrestin2 in striatum neurons dramatically enhanced the severity of dyskinesia by LBPM.
Drug screening revealed that 2-aminoethoxydiphenyl borate (2-ABP), nifedipine, nimodipine, flunarizine and ethoxzolamide significantly decreased abnormal movements in unc-77(e625) animals.
We found that LBPM developed less AIM severity compared with standard L-dopa administration, whereas selective deletion of β-arrestin2 in striatum neurons dramatically enhanced the severity of dyskinesia by LBPM.
Effects of linarin on treating AD zebrafish dyskinesia and AChE inhibition were compared with donepezil (DPZ) which was used as a positive control drug.