| Popis: |
Evidence presented from several studies suggests that dopamine deficiency may play a significant role not only in Parkinson's disease (PD) but also in encephalitis lethargica, multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS). It seems, however, that attempts to correct these deficiencies with high doses of levodihydroxyphenylalanine ( l -DOPA), while initially very beneficial, soon produce a wide range of adverse side effects. This chapter establishes why this is the case and how it may be possible to prevent, or at least reduce, l -DOPA's unwanted negative effects. The most logical explanation of the l -DOPA experience is that the damaging side effects of l -DOPA's use stem not directly from the drug but from its oxidation products. These include dopachrome and other chrome indoles that are hallucinogenic, toxic to neurons, and known to hasten death in Parkinsonism patients. It has been hypothesized from various studies that schizophrenics overproduce adrenochrome, adrenolutin, and other oxidation products of adrenaline, which, in turn, causes their illness. The presence of fluid-filled brain ventricles in chronic schizophrenia has been linked to levels of the important antioxidant enzyme glutathione peroxidase. The evidence presented in the chapter suggests that genetic aberrations, in certain individuals, promote the overproduction of the metabolites of adrenaline, adrenochrome, and its derivatives. As a result, such patients suffer from both the schizophrenogenic effects of these hallucinogens and the cumulative impacts of associated oxidative stress (OS). |
