Evaluation of Interleukins, ACTH, Cortisol and Prolactin Concentrations in the Blood of Patients with Parkinson's Disease

Parkinson''s disease (PD) is characterized by a markedly decreased number of nigrostriatal dopaminergic neurons. The pathogenesis of PD is still unknown; among other etiological factors, immunological abnormalities have been suggested. Recently, interleukin-2 (IL-2) has been hypothesized t...

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Bibliographic Details
Published in:Neuroimmunomodulation 1996-03, Vol.3 (2-3), p.131-134
Main Authors: Stypuła, Grażyna, Kunert-Radek, Jolanta, Stępień, Henryk, Żylińska, Krystyna, Pawlikowski, Marek
Format: Article
Language:English
Subjects:
Adrenocorticotropic Hormone - blood
Dopamine - physiology
Female
Humans
Hydrocortisone - blood
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - secretion
Interleukin-1 - blood
Interleukin-2 - blood
Interleukin-6 - blood
Interleukins - blood
Male
Middle Aged
Original Paper
Parkinson Disease - blood
Parkinson Disease - drug therapy
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - secretion
Prolactin - blood
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Summary:Parkinson''s disease (PD) is characterized by a markedly decreased number of nigrostriatal dopaminergic neurons. The pathogenesis of PD is still unknown; among other etiological factors, immunological abnormalities have been suggested. Recently, interleukin-2 (IL-2) has been hypothesized to be an endogenous cytokine that regulates striatal dopaminergic function. We examined the plasma concentrations of IL-1, IL-2, IL-6 and blood levels of ACTH, Cortisol and prolactin of 21 patients with PD without any previous treatment. Age-and sex-matched subjects without any neurological or immune disorders were used as controls. Significantly higher serum concentrations of IL-2 in patients with PD were found. Treatment with antiparkinsonian drugs reduced IL-2 levels in these patients. Our results suggest a functional relationship between central dopaminergic and immune systems and a possible involvement of the latter in the pathogenesis of PD.
ISSN:1021-7401
1423-0216
DOI:10.1159/000097237