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 t
he progression of neurological deficits in PD and the cognitive declin
e in AD. The immune response to bacterial or viral infection and in ch
ronic inflammatory processes is stimulated by an increased synthesis o
f the cytokines interleukin-1 beta (IL-1 beta) and subsequently interl
eukin-6 (IL-6). We investigated the influence of Selegiline on the syn
thesis of IL-1 beta and IL-6 in peripheral blood mononuclear cells (PB
MC) 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). Tre
atment of cultured PBMC with Selegiline significantly increased synthe
sis of both cytokines. The effect of Selegiline on cytokine biosynthes
is may contribute to its putative neuroprotective properties.