The conference entitled "Sphingolipids as Signaling Modulators in the Nervous System" will take place from July 13-17, 1997, at the New York University School of Law, New York City. The involvement of sphingolipids in processes such as neuronal differentiation, regeneration, and trophic assisted cell survival has been shown to include a number of signal transduction mechanisms as well as protein modulatory effects. Sphingomyelinase, for example, when activated by cytokines such as tumor necrosis factor, converts sphingomyelinase to ceramide which then functions as a active second messenger to trigger such processes as proliferation and apoptotic cell death. Sphingosine, sphingosine phosphate, and ceramide phosphate are also recognized as intracellular messengers exerting a variety of effects on cell proliferation and differentiation. Gangliosides, a class of sphingolipids, are well recognized neurotrophic factors which function as neuroprotective agents in a variety of in vitro and in vivo systems. Numerous studies have indicated their role as modulatory agents to a variety of membrane enzymes, receptors, ion channels and adhesion factors. They are now being actively studied as potential pharmaceutical agents for the treatment of specific neurological disorders including Parkinson's disease, spinal chord injury, and stroke. As a satellite to the biannual meeting of the International Society for Neurochemistry, the New York Academy of Sciences is sponsoring the "Sphingolipids as Signaling Modulators in the Nervous System" conference. Investigators will present the results of ongoing clinical trial employing GM1 ganglioside for the treatment of Parkinson's disease, spinal chord injury, and stroke, with a critical discussion of this approach to therapy. Presentations from basic scientists on the biochemical/cell biological aspects of gangliosides and other sphingolipids will focus on possible mechanisms to account for the trophic, neuroprotective properties of these substance. The immunogenic potential of gangliosides and sulfated glycosphingolipids for promoting neurological dysfunction will be explored, raising the key question of whether of not this invalidates their use as therapeutic agents. Ample time will be provided during the meeting for stimulating interchanges between research scientists and clinicians concerning basic mechanisms and the biomedical potential of sphingolipids.
|Effective start/end date||7/1/97 → 6/30/98|
- National Institutes of Health