ABSTRACT
The etiology of Parkinson’s disease and mechanism of nigrostriatal dopaminergic neurodegeneration remains elusive. The biochemical studies so far done on the substantia nigra pars compacta (SNPC) of Parkinson’s disease (PD) and the striatum from 6-hydroxydopamine-N-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP)-treated mice point to an ongoing biochemical process of abnormal iron metabolism within the reactive microglia and melanin-containing dopamine (DA) neurons, resulting in oxidative stress and inflammation that propagates the degeneration of the DA neurons.1-3. Both neurotoxins are considered to be relevant models of the disease and are thought to induce neurodegeneration via oxidative stress (OS) since iron chelator (e.g. desferrioxamine and R-apomorphine) and radical scavenger (vitamin E, ebselen, lipoic acid) pretreatment induces neuroprotection against the two neurotoxins.4,5 However, it is not known whether these are primary or secondary events. It is most likely that a cascade of biochemical events, similar to a domino effect, takes place, resulting eventually in the death of DA neurons. Many of these processes are not established or known.
