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Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms
Increased D1 dopamine receptor signaling in levodopa‐induced dyskinesia
The data suggest that levodopa‐induced dyskinesia results from increased dopamine D1 receptor–mediated transmission at the level of the direct pathway.
Electrophysiological and metabolic evidence that high‐frequency stimulation of the subthalamic nucleus bridles neuronal activity in the subthalamic nucleus and the substantia nigra reticulata
- C. Tai, T. Boraud, E. Bézard, B. Bioulac, C. Gross, A. Benazzouz
- BiologyFASEB journal : official publication of the…
- 1 October 2003
The hypothesis that HFS exerts an inhibitory influence on STN neuronal firing is supported and Electrophysiological and metabolic evidence that high‐frequency stimulation of the subthalamic nucleus bridles neuronal activity in the subhalamic nucleus and the substantia nigra reticulata is found.
Molecular mechanisms of l-DOPA-induced dyskinesia.
Attenuation of levodopa-induced dyskinesia by normalizing dopamine D3 receptor function
Results indicated that the D3 receptors participated in both dyskinesia and the therapeutic action of levodopa, and that partial agonists may normalize D3 receptor function and correct side effects of levidopa therapy in patients with Parkinson disease.
Pathophysiology of levodopa-induced dyskinesia: Potential for new therapies
Increased understanding of levodopa-induced dyskinesia is not only valuable for improving patient care, but also in providing new insights into the functional organization of the basal ganglia and motor systems.
Prototypic and Arkypallidal Neurons in the Dopamine-Intact External Globus Pallidus
The data support the concept that a dichotomous functional organization, as actioned by arkypallidal and prototypic neurons with specialized molecular, structural, and physiological properties, is fundamental to the operations of the dopamine-intact GPe.
The dopamine D3 receptor: a therapeutic target for the treatment of neuropsychiatric disorders.
- P. Sokoloff, J. Díaz, C. Gross
- Biology, PsychologyCNS & neurological disorders drug targets
- 31 January 2006
The D(3) receptor mediates behavioral abnormalities elicited by glutamate/NMDA receptor blockade, which suggests D(2) receptor-selective antagonists as novel antipsychotic drugs and novel treatment options in PD, schizophrenia and drug addiction, which are awaiting evaluation in clinical trials.
Loss of P-type ATPase ATP13A2/PARK9 function induces general lysosomal deficiency and leads to Parkinson disease neurodegeneration
- B. Dehay, A. Ramírez, E. Bézard
- Biology, ChemistryProceedings of the National Academy of Sciences
- 30 May 2012
It is shown that PD-linked mutations in ATP13A2 lead to several lysosomal alterations in PD patient-derived fibroblasts, including impaired lyssomal acidification, decreased proteolytic processing of lysOSomal enzymes, reduced degradation of lYSosomal substrates, and diminished lysoomal-mediated clearance of autophagosomes.
Lewy body extracts from Parkinson disease brains trigger α‐synuclein pathology and neurodegeneration in mice and monkeys
Supporting this concept, intracerebral inoculation of synthetic recombinant α‐synuclein fibrils can trigger α‐Synuclein pathology in mice, and it remains uncertain whether the pathogenic effects of recombinant synthetic α‐ synuclein may apply to PD‐linked pathological α‐ Synuclein and occur in species closer to humans.