The Role of Monoamine Oxidase B Inhibitors in the Treatment of Parkinson's Disease - An Update

• Published in: CNS & neurological disorders drug targets Vol. 22; no. 3; p. 329
• Main Authors: Chew, Zhi Xin, Lim, Chooi Ling, Ng, Khuen Yen, Chye, Soi Moi, Ling, Anna Pick Kiong, Koh, Rhun Yian
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01-01-2023
• Subjects: Antiparkinson Agents - pharmacology; Antiparkinson Agents - therapeutic use; Dopamine; Dopamine Agents; Humans; Monoamine Oxidase - metabolism; Monoamine Oxidase Inhibitors - pharmacology; Monoamine Oxidase Inhibitors - therapeutic use; Neurodegenerative Diseases; Parkinson Disease - drug therapy; Selegiline - pharmacology; rasagiline; safinamide; monoamine oxidase B inhibitor; neuroprotective; Parkinson’s disease; selegiline
• ISSN: 1996-3181
• DOI: 10.2174/1871527321666211231100255

Parkinson's disease (PD) is a progressive neurodegenerative disease characterised by reduced dopamine levels in the substantial nigra. This may lead to typical motor features such as bradykinesia, resting tremors and rigid muscles, as well as non-motor symptoms such as neuropsychiatric symptoms, sleep disorders, autonomic dysfunction, and sensory disturbances. Inhibitors of monoamine oxidase B (MAO-B) are used to alleviate symptoms by reducing monoamine oxidase-catalysed degradation of dopamine; hence, preserving functional levels of dopamine. The very first MAO-B inhibitor used therapeutically was selegiline, followed by rasagiline, its indane derivative which has superior efficacy and selectivity. Both inhibitors can be used as monotherapy or in combination with other anti- Parkinson drugs. Safinamide, a reversible MAO-B inhibitor that utilises both dopaminergic and non-dopaminergic mechanisms, was recently approved by the European Medicines Agency (EMA) (2015) and U.S. FDA (2017) as an add-on therapy for patients with mid- or late-stage Parkinson's disease. Furthermore, MAO-B inhibitors were found to be associated with potential neuroprotective and disease modifying effects. However, evidence of their efficacy and role in PD models is scarce and warrants further investigation.