Neuroinflammation and Dyskinesia: A Possible Causative Relationship?
Antonella CardinaleAntonio de IureBarbara PicconiPublished in: Brain sciences (2024)
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.
Keyphrases
- inflammatory response
- lipopolysaccharide induced
- gene expression
- lps induced
- cerebral ischemia
- end stage renal disease
- traumatic brain injury
- induced apoptosis
- ejection fraction
- newly diagnosed
- chronic kidney disease
- cognitive impairment
- dna methylation
- peritoneal dialysis
- parkinson disease
- prognostic factors
- cell cycle arrest
- physical activity
- high glucose
- cell proliferation
- deep brain stimulation
- stem cells
- toll like receptor
- diabetic rats
- prefrontal cortex
- neuropathic pain
- endothelial cells
- endoplasmic reticulum stress
- brain injury
- signaling pathway
- spinal cord injury
- drug delivery
- drug induced
- combination therapy
- spinal cord
- mesenchymal stem cells