Abstract
Levodopa (LD) is the most effective drug in the treatment of Parkinson’s disease (PD). However, although it represents the “gold standard” of PD therapy, LD can cause side effects, including gastrointestinal and cardiovascular symptoms as well as transient elevated liver enzyme levels. Moreover, LD therapy leads to LD-induced dyskinesia (LID), a disabling motor complication that represents a major challenge for the clinical neurologist. Due to the many limitations associated with LD therapeutic use, other dopaminergic and non-dopaminergic drugs are being developed to optimize the treatment response. This review focuses on recent investigations about non-dopaminergic central nervous system (CNS) receptor ligands that have been identified to have therapeutic potential for the treatment of motor and non-motor symptoms of PD. In a different way, such agents may contribute to extending LD response and/or ameliorate LD-induced side effects.
Highlights
Parkinson’s disease (PD), known as idiopathic paralysis agitans, is one of the most frequent chronic neurodegenerative diseases worldwide
To help researchers in such a challenge, this review focuses on recent investigations about non-dopaminergic central nervous system (CNS) receptor ligands that have been identified to have therapeutic potential for the treatment of motor and non-motor symptoms of PD
It can indirectly modulate GABA, serotonin and glutamate indicates the possible presence of other subunits in the receptor complex) are mainly implicated in release, since nicotinic receptors are localized on GABAergic, serotoninergic and glutamatergic mediating both neuroprotective and antidyskinetic effects, suggesting that nicotinic subtype selective interneurons [299,300]
Summary
Parkinson’s disease (PD), known as idiopathic paralysis agitans, is one of the most frequent chronic neurodegenerative diseases worldwide. Its etiology has not been determined so far, the main pathological characteristic is the decrease of the dopamine (DA) level due to the degeneration of the dopaminergic neurons in the substantia nigra pars compacta [1,2] This leads to motor (i.e., postural instability, dyskinesias, tremor, and rigidity) and non-motor (i.e., depression, cognitive impairment, pain, hallucinations) symptoms [3,4,5,6,7,8,9,10,11,12,13].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
