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Levodopa-induced Dyskinesia in Parkinson’s Disease: Plausible Inflammatory and Oxidative Stress Biomarkers

Published online by Cambridge University Press:  20 January 2023

Swagata Sarkar
Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India Department of Physiology, University of Calcutta, Kolkata, India
Akash Roy
Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India Department of Physiology, University of Calcutta, Kolkata, India
Supriyo Choudhury
Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India
Rebecca Banerjee
Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India
Sanjit Dey
Department of Physiology, University of Calcutta, Kolkata, India
Hrishikesh Kumar*
Department of Neurology, Institute of Neurosciences Kolkata, Kolkata, India
Corresponding author: Dr Hrishikesh Kumar, Head, Department of Neurology, Institute of Neurosciences Kolkata, 185/1, A.J.C Bose Road, Kolkata- 700017, West Bengal, India. Email:



Pathophysiology of levodopa-induced dyskinesia (LID) remains obscure. Increased dopamine metabolism due to prolonged levodopa treatment can exacerbate oxidative damage and neuroinflammatory pathology in Parkinson’s disease (PD). Association of novel peripheral markers with LID severity might provide insight into LID pathomechanisms.


We aimed to study specific peripheral blood inflammatory-oxidative markers in LID patients and investigate their association with clinical severity of LID.


Motor, non-motor and cognitive changes in PD with and without LID compared to healthy-matched controls were identified. Within the same cohort, inflammatory marker (sLAG3, TOLLIP, NLRP3 and IL-1β) levels and antioxidant enzyme activities were determined by ELISA and spectrophotometric methods.


LID patients showed distinctly upregulated TOLLIP, IL-1β levels with significant diminution of antioxidant activity compared to controls. Significant negative association of cognitive markers with oxidative changes was also observed.


To our understanding, this is the first study that indicates the involvement of toll-like receptor-mediated distinct and low-grade inflammatory activation in LID pathophysiology.

Résumé :


Dyskinésie provoquée par la lévodopa : présence possible de biomarqueurs de stress oxydatif et d’inflammation.

Contexte :

On ne connaît pas très bien la physiopathologie de la dyskinésie provoquée par la lévodopa (DPL). Il se peut que l’augmentation du métabolisme de la dopamine due à un traitement prolongé par la lévodopa aggrave le stress oxydatif et le processus neuro-inflammatoire dans la maladie de Parkinson (MP). L’établissement d’une association de nouveaux marqueurs périphériques avec le degré de gravité de la DPL pourrait jeter un certain éclairage sur les mécanismes pathologiques de ce trouble d’exécution des mouvements.

Objectifs :

L’étude visait à détecter la présence de certains marqueurs de stress oxydatif et d’inflammation dans le sang périphérique, chez des patients présentant une DPL, et à examiner l’association de cette présence avec le degré de gravité clinique du trouble.

Méthode :

Une comparaison a été établie entre les changements moteurs, non moteurs et cognitifs notés chez des patients atteints de la MP, présentant ou non une DPL, et les résultats obtenus chez des témoins appariés, en bonne santé. Les taux de marqueurs d’inflammation (sLAG3, TOLLIP, NLRP3 et IL1-1β) et le degré d’activité enzymatique antioxydante ont été déterminés, dans la même cohorte, par la méthode ELISA et par spectrophotométrie.

Résultats :

Comparativement aux témoins, les patients atteints d’une DPL avaient une augmentation notable des taux de TOLLIP et d’IL1-1β, accompagnée d’une diminution importante de l’activité antioxydante. Une association négative significative a également été notée entre les marqueurs cognitifs et les changements oxydatifs.

Conclusion :

À notre connaissance, il s’agirait de la première étude dans laquelle les auteurs font état d’une activité inflammatoire de faible intensité, distincte, médiée par les récepteurs Toll (TLR) dans la physiopathologie de la DPL.

Original Article
© The Author(s), 2023. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation

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SS and AR contributed equally to this research.


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