Depression in Parkinson's disease

Selegiline stimulates biosynthesis of cytokines interleukin-1 beta and interleukin-6

Wilfried K, Muller T, Kruger R, Horst P

Department of Neurology,
St. Josef-Hospital,
University of Bochum, Germany.
Neuroreport 1996 Nov 25; 7(18):2847-8

ABSTRACT

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.

Parkinson's research / abstracts

1.    Deprenyl effect on cognitive functions in early Parkinson's
2.    Deprenyl depression in Parkinson's disease
3.    Deprenyl stimulates biosynthesis of cytokines interleukin-1 & 6
4.    Deprenyl effect of MAO-B inhibitors on MPP+ toxicity
5.    Deprenyl modulates the decline of the dopamineric system
6.    Deprenyl possible mechanisms of action in Parkinson's
7.    Deprenyl pharmacological basis of the beneficial effects
8.    Deprenyl improves visuo-motor control in early Parkinsonism
9.    Deprenyl delays disability in Parkinsonian patients
10.   Deprenyl management of early Parkinson's disease
11.   Deprenyl delays the onset of disability in Parkinsonian patients
12.   Deprenyl and tocopherol antioxidative therapy of Parkinsonism