Abstract
Evidence is presented to show that in Parkinson’s disease (PD) there exists a topographical degeneration in the nigrostriatal dopamine system. This finding may account for response variabilities and side effects occuring after antiparkinsonian therapy. Postsynaptic receptors do not show topical differences in both Bmax- and KD-values in treated PD. Postsynaptic receptors respond inadequately in about 30% of PD. Denervation supersensitivity may only occur in striatal subareas depleted of dopamine to an extent of > 90%. Compensatory mechanisms include presynaptic overactivity and enhanced activity of otherwise reduced tyrosine hydroxylase. Iron (III), total iron and ferritin are significantly increased in the substantia nigra indicating disturbances at the level of redox-equilibrium, respiratory chain activity and energy metabolism. These findings together with accumulation of exogenous or endogenous toxins may be of pathogenic importance in PD. Whether such pathophysiological considerations involve peripheral dopamine or catecholaminergic systems (e.g. the sympatho-adrenal medullary function) is uncertain and requires further experimental studies.
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