M. K. Mazumder

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Cerebral ischemia (CI), caused by the deprivation of oxygen and glucose to the brain, is the leading cause of permanent disability. Neuronal demise in CI has been linked to several pathways which include cyclooxygenases (COX) - mediated production of prostaglandins (PGs) and subsequently reactive oxygen species (ROS), aquaporin-4 (AQ-4) - mediated brain(More)
While the cause of dopaminergic neuronal cell death in Parkinson’s disease (PD) is not yet understood, many endogenous molecules have been implicated in its pathogenesis. β-phenethylamine (β-PEA), a component of various food items including chocolate and wine, is an endogenous molecule produced from phenylalanine in the brain. It has been reported recently(More)
Hyperactivation of GluN2B subunit containing N-methyl-d-aspartate receptors (NMDARs) significantly contributes to the development of several neurodegenerative diseases through a process called excitotoxicity. NMDARs are voltage-gated Ca2+ channels which when activated lead to excessive influx of Ca2+ into neurons thereby exacerbating several(More)
One of the intermediates of methionine cycle, the homocysteine (Hcy), elevates in plasma of Parkinson's disease (PD) patients undergoing L-DOPA (3,4-dihydroxyphenylalanine) therapy and has been regarded as a risk factor of the disease. Several evidences pointed out that Hcy causes degeneration of dopaminergic neurons. In rodent, elevated level of Hcy in(More)
Inhibition of catechol-O-methyltransferase (COMT), with drugs like tolcapone and entacapone, has been in practice to reduce L-DOPA-induced hyperhomocysteinemia in Parkinson’s disease (PD) patients. During L-DOPA methylation, S-adenosylhomocysteine is produced which is further processed to synthesize homocysteine (Hcy). Hcy has been reported to cause(More)
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