Selegiline stimulates biosynthesis of cytokines interleukin-1 beta and interleukin-6
Wilfried K, Muller T, Kruger R, Horst P
Department of Neurology,
University of Bochum, Germany.
Neuroreport 1996 Nov 25; 7(18):2847-8
Several lines of evidence indicate an immune-mediated pathophysiology of Parkinson's disease (PD) and Alzheimer's disease (AD).
In clinical studies the monoamine oxidase-B inhibitor Selegiline appears to slow the progression of neurological deficits in PD and the cognitive decline in AD.
The immune response to bacterial or viral infection and in chronic inflammatory processes is stimulated by an increased synthesis of the cytokines interleukin-1 beta (IL-1 beta) and subsequently interleukin-6 (IL-6).
We investigated the influence of Selegiline on the synthesis of IL-1 beta and IL-6 in peripheral blood mononuclear cells (PBMC) from healthy blood donors cultured with or without Selegiline (10(-8)M, 10(-9)M or 10(-10)M) in a humidified atmosphere (7% CO2). Treatment of cultured PBMC with Selegiline significantly increased synthesis of both cytokines.
The effect of Selegiline on cytokine biosynthesis may contribute to its putative neuroprotective properties.
research / abstracts
effect on cognitive functions in early Parkinson's
depression in Parkinson's disease
stimulates biosynthesis of interleukin-1 & 6
effect of MAO-B inhibitors on MPP+ toxicity
modulates the decline of the dopamineric system
mechanisms of action in Parkinson's
basis of the beneficial effects
visuo-motor control in early Parkinsons
in Parkinsonian patients
early Parkinson's disease
delays the onset
of disability in Parkinsons patients
antioxidative therapy of Parkinsonism