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This review explores the roles of NF\u2010\u03baB and TNF\u2010\u03b1 signalling pathways in LID pathophysiology and potential therapeutic approaches targeting these mechanisms. Chronic levodopa treatment leads to aberrant neuroplasticity and neuroinflammation, involving activation of NF\u2010\u03baB and increased production of pro\u2010inflammatory cytokines like TNF\u2010\u03b1. NF\u2010\u03baB activation in glial cells contributes to sustained neuroinflammation and exacerbates dopaminergic neuron loss. TNF\u2010\u03b1 levels are elevated in brain regions affected by LID and correlate with dyskinesia severity. Several compounds are involved in mitigating LID by modulating these pathways. Agmatine reduces NF\u2010\u03baB activation and NMDA receptor expression while protecting dopaminergic neurons. Resveratrol and doxycycline demonstrate antidyskinetic effects by attenuating neuroinflammation and TNF\u2010\u03b1 production. The Rho\u2010kinase (ROCK) inhibitor fasudil and cannabinoid receptor 2 (CB2) receptor agonists also show efficacy in reducing LID severity and neuroinflammation. Hydrogen gas inhalation decreases pro\u2010inflammatory cytokine levels associated with LID. These findings highlight the complex interplay between NF\u2010\u03baB, TNF\u2010\u03b1 and other neurotransmitter systems in LID pathogenesis. Targeting neuroinflammation and glial activation through these pathways represents a promising strategy for developing novel LID treatments. Further research is needed to fully elucidate the mechanisms and optimize therapeutic approaches targeting NF\u2010\u03baB and TNF\u2010\u03b1 signalling in LID.<\/jats:p>","DOI":"10.1111\/ejn.70034","type":"journal-article","created":{"date-parts":[[2025,3,12]],"date-time":"2025-03-12T01:32:03Z","timestamp":1741743123000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The Roles of Neuroinflammation in\n                    <scp>l<\/scp>\n                    \u2010DOPA\u2010Induced Dyskinesia: Dissecting the Roles of NF\u2010\u03baB and TNF\u2010\u03b1 for Novel Pharmacological Therapeutic Approaches"],"prefix":"10.1111","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0944-0320","authenticated-orcid":false,"given":"Mohammad\u00a0Yasin","family":"Zamanian","sequence":"first","affiliation":[{"name":"Neurophysiology Research Center Hamadan University of Medical Sciences  Hamadan Iran"},{"name":"Department of Pharmacology and Toxicology, School of Pharmacy Hamadan University of Medical Sciences  Hamadan Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maryam","family":"Golmohammadi","sequence":"additional","affiliation":[{"name":"School of Medicine Shahid Beheshti University of Medical Sciences  Tehran Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhanna\u00a0R.","family":"Gardanova","sequence":"additional","affiliation":[{"name":"Pirogov Russian National Research Medical University  Moscow Russia"},{"name":"Medical University MGIMO\u2010MED  Moscow Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohammad","family":"Rahimi","sequence":"additional","affiliation":[{"name":"Student Research Committee Hamadan University of Medical Sciences  Hamadan Iran"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lusine\u00a0G.","family":"Khachatryan","sequence":"additional","affiliation":[{"name":"Department of Pediatric Diseases, N.F. 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