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Levodopa is the principal agent in the treatment of Parkinson's disease (PD). Unfortunately the therapeutic benefits are optimal only in the early stages of the disease, with long-term use associated with motor complications such as levodopa-induced dyskinesia (LID). Risk factors associated with the development of LID are generally accepted to involve the degree of dopamine (DA) denervation in the nigrostriatal pathway, levodopa dose, and duration of levodopa treatment. Little is known regarding the underlying mechanisms of LID, although it is known that levodopa plasma concentrations are closely associated with the onset of some types of LIDs (peak-dose and biphasic dyskinesias) and it appears that increased DA turnover plays a crucial role in LID development. Recent evidence suggests that other cell types such as serotonin neurons possess the ability to convert levodopa into DA, subsequently storing and releasing it thereby increasing the levels of extracellular DA, exacerbating LID. This review will highlight the evidence to date from in vitro and in vivo studies utilizing both animal models and patients, regarding the relationship between levodopa treatment and the development of LID. Understanding the pathogenesis of LID is a therapeutic priority in tackling motor complications related to levodopa treatment in PD.


Journal article


European Neurological Journal

Publication Date





20 - 26