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Hi, yesterday I was on a Symposium in Bad Nauheim/Germany. There was speaking Prof. Dr. Moussa B.H. Youdin from Haifa. This is his opinion: . Bad Nauheimer Parkinson-Symposlum 16. Januar 1999 Prof Dr Moussa B.H. Youdim . Is Neuroprotection possible in Parkinson 's Disease? Moussa B.H. Youdim, Technion-Israel Institute of Technology, Faculty of Medicine, Eve Topf and USA national Parkinson Foundation Centers of.Excellence for Neurodegenerative Diseases Research, Haifa, Israel and Fogarty International Center for Advanced Studies in Medical Sciences, NIH Bethesda, USA. In Parkinson 's Disease (PD) the pigmented melanin containing dopamine neurons arising in the raphae nucleus and terminating in the striatum (nigro- striatal) degenerate. Although the etiology of PD is not known, a significant body of evidence that point to a selective on going process of excessive oxygen radical species (superoxide, nitric oxide and reactive hydroxyl radical) generation, resulting in oxidative stress (OS) in the substantia nigra pars compacta (SNPC). The main feature of OS are increased inflammatory responses which expresses itself by increases in TFN-alpha, IL-1, IL-6 and TGf-beta and acitvated microglia and increases of iron, ferritin, monoamine oxidase B Activity, ubiquitination, lipofuscin deposition and lipid peroxidation. There are also decreases of recluced glutathion (GSH), calcium binding protein and mitochondrial electron transport enzymes which get rid of ORS. It is more than interesting that in the animal models of PD, the neurotoxins MPTP and 6-hydroxydopamine produce their degeneration of nigro-striatal dopamine neurons via a mechanism involving ORS induced OS with similar biochemical changes that have been described in idiopathic parkinsonism. Thus animal models are being used as means to develop drugs that would protect against an on going progressive neurodegeneration. These models have indicated that ORS scavengers and iron chelators may have a potential as neuroprotective drugs, not only in PD, but other neurodegenrative diseases such as Alzheimer 's disease where the same mechanisms are being described. A number of studies have been done with I-selegiline and vitamin E but sofar their neuroprotective activity has been inconclusive. We have evidence that suggests iron accumulation in PD brains has a pivotal role in the process of neurodegeneration. For these reasons we have been searching for non-toxic iron chelators for the treatment of PD similar to the use of copper chelators for the treatnent of Wilson 's Disease. Of the drugs examined, we have shown that apomorphine (a drug first synthesized in Germany 135years ego) , the antiparkinson dopamine DI-D2 receptor agonist, is one of most potent iron chelators so far described. Apomorphine protects dopamine neurons death as induced by neurotoxins (MPTP, 6-hydoxydopamine and iron) in vitro, in vivo and in cell culture experiments. We know of no other presently available anti PD drug which has the neuroprotective actions of apomorphine in animal models of PD. Thus apomorphine may be the most ideal drug available for clinical neuroprotection. Recent long term clinical studies in Europe with apomorphine is showing remarkable action, namely that long term parkinsonian apomorphine users are stabilized and can be weaned of L-dopa. The question to be investigated is whether in such patients apomorphine is showing europrotection and slowing the progression of the disease. This is now been investigated clinically by our group in collaboration with Prof. Poewe (Austria) and Prf Leenders (Holland) using PET and SPECT.