Neuropharmacology And NeurotoxicologyImmunosuppressant FK506 does not exert beneficial effects in symptomatic G93A superoxide dismutase-1 transgenic miceAnneser, Johanna M. H.; Gmerek, Andreas1; Gerkrath, Jasmin1; Borasio, Gian DomenicoCA; Heumann, Rolf1Author Information Department of Neurology, Ludwig-Maximilians-University, Klinikum Grosshadern, D-81366 Munich; 1Department of Molecular Neurobiochemistry, Ruhr-University, Bochum, Germany CACorresponding Author Received 23 May 2001; accepted 13 June 2001 Neuroreport: August 28th, 2001 - Volume 12 - Issue 12 - p 2663-2665 Buy SDC Abstract The immunosuppressant drug FK506 has been shown to exert neuroprotective effects in various model systems via inhibition of the protein phosphatase calcineurin (CN). The enzyme Cu/Zn-superoxide dismutase (SOD1), which is mutated in a familial form of amyotrophic lateral sclerosis (ALS), is an endogenous regulator of CN. Altered function of CN may therefore be involved in the pathogenesis of ALS. We tested FK506 in a transgenic mouse model expressing mutated SOD1 for potential beneficial effects. This treatment, initiated after onset of symptoms, did not cause a reduction in the decline of motor function nor did it prolong survival. These results argue against a crucial role of CN in the process leading to motoneuronal degeneration in SOD1-mutated mice. © 2001 Lippincott Williams & Wilkins, Inc.