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Abstract
Parkinsonism was first described in 1817, by James Parkinson. It is caused by lesions n the basal ganglia, particularly, the substantia nigra pars compacta.
There are many causes of parkinsonism; among which, idiopathic parkinsonism or Parkinson’s disease (PD) is the commonest.
Drugs (e.g. neuroleptics) and chemical toxins arc also common causes of secondary Parkinsonism. It may appear as a manifestation in other neurodegenrative diseases.
Genetic factor is suspected among the pathogenetic mechanisms.
The core biochemical pathology in parkinsonism is decreased dopaminergic neurotransmission in the basal ganglia. Mitochondrial respiratory chain dysfunction, and defect in the natural metabolic pathway (monoamine oxidase) that clears the neurotransmitters form the dopaminergic neurons, have been implicated as the main pathogenetic factors in Parkinsonism; as they are major sources of reactive oxygen species, supporting the concept that oxidative stress is wildly involved in nigral cell degeneration in Parkinsonism.
A lot of studies suggest that misrcgulalion of iron metabolism, iron-induced oxidative stress, and free radial formation are major pathogenic factors in PI) and the other related neurodegenerative disorders.
In the present study, we assessed the activities of the mitochondrial respiratory chain cir/ymes and monoaminc-B oxidase in neutrophils. Also, we assessed the plasma levels of iron, total iron binding capacity, and ferritin. Subjects included in this study were divided into 3 groups. Group 1 included 20 patients diagnosed as idiopathic parkinsonism. p’rnim H inHnHfd 90 oatients having major psychotic disorders and