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
- gene expression
- lipopolysaccharide induced
- lps induced
- cerebral ischemia
- end stage renal disease
- traumatic brain injury
- chronic kidney disease
- induced apoptosis
- newly diagnosed
- ejection fraction
- cognitive impairment
- dna methylation
- peritoneal dialysis
- parkinson disease
- subarachnoid hemorrhage
- cell cycle arrest
- high glucose
- toll like receptor
- blood brain barrier
- brain injury
- spinal cord
- cell death
- patient reported outcomes
- cancer therapy
- cell proliferation
- spinal cord injury
- cell therapy
- pi k akt