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Background: Levetiracetam, a novel antiepileptic drug, has shown antidyskinetic effects in experimental animal models of Parkinson's disease (PD). The tolerability and efficacy of levetiracetam in reducing the levodopa-induced dyskinesia (LID) in PD patients have not been established. Therefore, this study aims to synthesize evidence from published prospective clinical trials about the efficacy of levetiracetam for the management of LID in PD patients. Methods: We followed the PRISMA statement guidelines during the preparation of this systematic review. A computer literature search of PubMed, EBSCO, Scopus, MEDLINE, and the web of science was carried out. We selected prospective clinical trials assessing the anti-dyskinetic efficacy of levetiracetam for treating LID in patients with PD. The Abnormal Involuntary Movement Scale (AIMS), Clinical Global Impression Score (GCI), UPDRS III, and UPDRS IV were considered as the primary outcome measures; their data were extracted and reviewed. Results: Our review included seven clinical trials with a total of 150 patients. Of them, three studies were randomized controlled trials, and the remaining were open-label single arm trials. Four studies reported poor tolerability of the levetiracetam with mild anti-dyskinetic effects. Levetiracetam slightly improved the UPDRS-IV and AIMS scores with small effect size. In the remaining three studies, levetiracetam failed to exhibit any anti-dyskinetic effects. Conclusion: Current evidence does not support the efficacy of the levetiracetam for treating LID in PD patients, however, due to the limited number of published randomized control trials (RCTs), further RCTs are required.

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Inflammation is considered an important aspect in the development of atherosclerosis. Genetic manipulations of animal models susceptible to atherosclerosis have unraveled the contribution of various inflammatory pathways implicated in the development of atherosclerosis. These inflammatory pathways not only lead to the recruitment and entry of inflammatory cells into the arterial wall, they also modify the morphology and composition of atherosclerotic plaques. Certain inflammatory pathways, such as P-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, appear to play an important role in lesion initiation, whereas others, such as interleukin-10 and CD40/CD40 ligand, seem to contribute to lesion progression and morphologic changes. An understanding of these pathways will allow the development of new strategies in the management of atherosclerosis. This review provides a roadmap for better utilization of these models in atherosclerosis research.

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