Tea and Parkinson's disease: Constituents of tea synergize with antiparkinsonian drugs to provide better therapeutic benefits.
The major neurodegenerative movement disorder Parkinson's disease (PD) is characterized by rest-tremor, akinesia, rigidity and inability to initiate movements. PD syndromes result from excessive loss of dopamine from the forebrain striatal region, due to dopaminergic neuronal death in the midbrain substantia nigra pars compacta. PD with multifactorial etiology is believed to ideally require a drug or different drugs that act(s) at multiple sites of action for symptomatic relief. Replenishing striatal dopamine by providing L-3,4-dihydroxyphenylalanine (l-DOPA) along with a peripheral aromatic amino acid decarboxylase inhibitor is the mainstay treatment for PD. Such prolonged therapy leads to debilitating effects, often worsening the affection. Interestingly some under-appreciated pharmaceutical compounds, including constituents of plants and nutraceuticals can synergize with l-DOPA to support mitochondrial function, suppress inflammation, ease oxidative stress, and in turn slow the progression of the disease. Tea and other dietary polyphenols are shown to provide relief to the disease syndromes and provide neuroprotection in cellular and animal models of PD. At par with these findings, random epidemiological studies in certain populations of the world support habitual tea drinking to reduce the risk of PD. The present review addresses how these tea constituents work at the cellular level to render effective control of the disease syndromes and suggests that tea synergizes with established drugs, such as l-DOPA to maximize their effects at certain levels in the disease phenotype-inducing canonical pathways of PD.
Division of Cell Biology & Physiology, CSIR-Indian Institute of Chemical Biology, 4, Raja Subodh Chandra Mullick Road, Kolkata 700032, India.
Debashis
D
Dutta
Division of Cell Biology & Physiology, CSIR-Indian Institute of Chemical Biology, 4, Raja Subodh Chandra Mullick Road, Kolkata 700032, India. Electronic address: mohankumar@iicb.res.in.
Kochupurackal P
KP
Mohanakumar
D000818:Animals; D000978:Antiparkinson Agents / Q000008:administration & dosage / Q000378:metabolism*; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000378:metabolism; D004357:Drug Synergism; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage / Q000378:metabolism; D010300:Parkinson Disease / Q000188:drug therapy* / Q000378:metabolism*; D059808:Polyphenols / Q000008:administration & dosage / Q000378:metabolism*; D013662:Tea / Q000378:metabolism*
D000978:Antiparkinson Agents; D059808:Polyphenols; D013662:Tea; D007980:Levodopa
Catechins; Catechol-O-methyl transferase inhibition; Phophorylated ERK1/2; Polyphenols; Rasagiline; Theoflavin