Neuroinflammation: Fanning the fire of <scp>l</scp>‐dopa‐induced dyskinesia

Bishop, Christopher

doi:10.1002/mds.27900

Cited by 8 publications

(6 citation statements)

References 21 publications

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“…This is in line with a recent report of a patient with worsening levodopa-induced dyskinesias after receiving the BNT162b2 (Pfizer/BioNTech) mRNA vaccine, 4 and preclinical studies supporting a role of neuroinflammation in levodopa-induced dyskinesia generally. 5 The unilateral symptomatology in our cases is interesting; however, similarly focal presentations in the setting of systemic autoimmune disorders, such as Sydenham's chorea, have been reported. 6 Alternatively, subclinical Parkinsonism affecting the contralateral side (case 1) could also have masked a bilateral process.…”

mentioning

confidence: 52%

Acute Hemichorea‐Hemiballismus Following COVID‐19 (AZD1222) Vaccination

et al. 2021

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confidence: 52%

Acute Hemichorea‐Hemiballismus Following COVID‐19 (AZD1222) Vaccination

et al. 2021

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“…In our MPTP-induced PD model, infiltration of inflammatory cells was found in the parenchymal striatum in the levodopa group, which is in accordance with previous studies showing that neuroinflammation could exacerbate levodopa-induced dyskinesia. 19 Inflammation has a pathogenic role in neurodegenerative diseases. Both dystonia and LID belong to hyperkinetic movement disorders.…”

Section: Discussionmentioning

confidence: 99%

Co-Application of C16 and Ang-1 Improves the Effects of Levodopa in Parkinson Disease Treatment

Fu¹,

Wang²,

Cai³

et al. 2022

JIR

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Background: Levodopa is regarded as a standard medication in Parkinson disease (PD) treatment. However, long-term administration of levodopa leads to levodopa-induced dyskinesia (LID), which can markedly affect patient quality of life. Previous studies have shown that neuroinflammation in the brain plays a role in LID and increases potential neuroinflammatory mediators associated with the side effects of levodopa. Objective: The treatment effect of C16 (a peptide that competitively binds integrin αvβ3 and inhibits inflammatory cell infiltration) and angiopoietin-1 (Ang-1; a vascular endothelial growth factor vital for blood vessel protection), along with levodopa, was evaluated in a rodent model of PD. Methods: We administered a combination of C16 and Ang-1 in a rodent model of PD induced by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Seventy-five mice were randomly divided into five treatment groups: control, vehicle, levodopa, C16 +Ang-1, and levodopa+C16+Ang-1. Behavioral, histological, and electrophysiological experiments were used to determine neuron function and recovery. Results: The results showed that C16+Ang-1 treatment alleviated neuroinflammation in the CNS and promoted the recovery effects of levodopa on neural function. Conclusion:Our study suggests that C16+Ang-1 can compensate for the shortcomings of levodopa, improve the CNS microenvironment, and ameliorate the effects of levodopa. This treatment strategy could be developed as a combinatorial therapeutic in the future.

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“…Moreover, treatment with MPEP (a metabotropic glutamate receptor 5 antagonist) reduced both the development of LID in de novo MPTP-lesioned monkeys and the inflammatory reaction measured by means of IBA1, CD68, and GFAP markers [88]. As is well known, PD is closely associated with advancing age and at the same time also affects Accumulating research evidence has demonstrated the inflammatory response contribution to LIDs by the contribution of microglia and soluble pro-inflammatory cytokines (TNF-α, Il-1β, iNOS) [20,86]. As demonstrated by Mulas and co-workers in 2016, a dyskinetic L-DOPA treatment also induced microglial reactivity with increased TNF-α expression in contrast to a different L-DOPA administration, defined non-dyskinetic, through continuous subcutaneous infusion [20,87].…”

Section: Neuroinflammation and Its Role In Lid Developmentmentioning

confidence: 99%

“…astrocytes also possess monoamine oxidase (MAO-B) and catechol-O-methyltransferase (COMT) and thus participate in L-DOPA metabolism [85]. Accumulating research evidence has demonstrated the inflammatory response contribution to LIDs by the contribution of microglia and soluble pro-inflammatory cytokines (TNF-α, Il-1β, iNOS) [20,86]. As demonstrated by Mulas and co-workers in 2016, a dyskinetic L-DOPA treatment also induced microglial reactivity with increased TNF-α expression in contrast to a different L-DOPA administration, defined non-dyskinetic, through continuous subcutaneous infusion [20,87].…”

Section: Neuroinflammation and Its Role In Lid Developmentmentioning

confidence: 99%

Neuroinflammation and Dyskinesia: A Possible Causative Relationship?

Cardinale,

de Iure,

Picconi

2024

Brain Sciences

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Levodopa (L-DOPA) treatment represents the gold standard therapy for Parkinson’s disease (PD) patients. L-DOPA therapy shows many side effects, among them, L-DOPA-induced dyskinesias (LIDs) remain the most problematic. Several are the mechanisms underlying these processes: abnormal corticostriatal neurotransmission, pre- and post-synaptic neuronal events, changes in gene expression, and altered plasticity. In recent years, researchers have also suggested non-neuronal mechanisms as a possible cause for LIDs. We reviewed recent clinical and pre-clinical studies on neuroinflammation contribution to LIDs. Microglia and astrocytes seem to play a strategic role in LIDs phenomenon. In particular, their inflammatory response affects neuron-glia communication, synaptic activity and neuroplasticity, contributing to LIDs development. Finally, we describe possible new therapeutic interventions for dyskinesia prevention targeting glia cells.

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Neuroinflammation: Fanning the fire of l‐dopa‐induced dyskinesia

Cited by 8 publications

References 21 publications

Acute Hemichorea‐Hemiballismus Following COVID‐19 (AZD1222) Vaccination

Acute Hemichorea‐Hemiballismus Following COVID‐19 (AZD1222) Vaccination

Co-Application of C16 and Ang-1 Improves the Effects of Levodopa in Parkinson Disease Treatment

Neuroinflammation and Dyskinesia: A Possible Causative Relationship?

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