Neuroprotective strategies to prevent and treat Parkinson’s disease based on its pathophysiological mechanism

• Published in: Archives of pharmacal research Vol. 40; no. 10; pp. 1117 - 1128
• Main Authors: Lee, Yujeong, Kim, Min-Sun, Lee, Jaewon
• Format: Journal Article
• Language: English
• Published: Seoul Pharmaceutical Society of Korea 01.10.2017; 대한약학회
• Subjects: agonists; Alzheimer disease; Cytokines - metabolism; dopamine; Dopaminergic Neurons - drug effects; Dopaminergic Neurons - immunology; drugs; etiology; Humans; Inflammation; L-dopa; Medicine; Membrane Potential, Mitochondrial - drug effects; Microglia - drug effects; Microglia - immunology; mitochondria; Neuroprotective Agents - therapeutic use; oxidative stress; Oxidative Stress - drug effects; Parkinson disease; Parkinson Disease - drug therapy; Parkinson Disease - etiology; Parkinson Disease - immunology; Pharmacology/Toxicology; Pharmacy; Plant Preparations - therapeutic use; Review; 약학; Pathophysiological pathway; Oxidative stress; Phytochemicals; Mitochondrial dysfunction; Neuroinflammation; Parkinson’s disease; Adaptive cellular stress response
• ISSN: 0253-6269; 1976-3786; 1976-3786
• DOI: 10.1007/s12272-017-0960-8

Parkinson’s disease (PD) is the second most common progressive neurodegenerative disease after Alzheimer’s disease. PD exhibits clinical symptoms that include tremors, rigidity, and bradykinesia. Many drugs are available to treat PD, such as, l -dopa, COMT inhibitor, MAO-B inhibitor, and dopamine agonists, but these drugs simply compensate for dopamine loss in PD, and therefore, cannot completely suppress its symptoms or progression. Although the causes of PD are not clearly understood, common pathophysiological pathways, such as, oxidative stress, mitochondrial dysfunction, and neuroinflammation are considered to be etiological factors, and thus, many treatments and interventions have been developed to target these pathophysiological factors. This review describes the neuroprotective strategies devised based on current understanding of the pathophysiological mechanisms of PD.