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Highlights of UPF Newsletter 1996-3 (United Parkinson Foundation, 833 W. Washington Blvd., Chicago, Illinois 60607): The letter reports two scientific meetings in Europe this summer, to discuss current research. Diagnosis: There is still no reliable way to distinguish PD from its numerous mimics, early enough to affect treatment or the conduct of trials. Tissue transplant: A German group has in two cases tried grafts of cells from the patient's omentum, a large apron-like structure in the intestinal cavity which happens to be rich in dopaminergic cells as well as neurotrophic factors. Benefits after a few months were comparable with those of embryonic transplants. Selegiline: Two studies found no significant mortality effect. While its benefit in PD is generally acknowledged, precisely how or why it works remains unknown. Deep Brain Stimulation (DBS, formerly VIM/STIM) is getting more popular, as researchers try new application sites in the brain. Pramipexole may have protective as well as symptomatic benefits, permitting decrease or delay of levodopa therapy in early stages. Levodopa, while effective against PD symptoms, is still suspected of being toxic in the long run. Bromocryptine and Pergolide both may have neuroprotective effect. Ropinirole, nearing approval stage, has had numerous trials to compare it against other drugs. Neurodegeneration is well known as the cause of PD, but the cause of neurodegeneration is a mystery. One hypothetical possibility is an endogenous toxin, possibly due to a metabolic error. Levodopa-induced dyskinesia is caused by a complex chain of effects involving NMDA (N-methyl-D-aspartate) receptors. NMDA antagonists relieve the dyskinesia, but unfortunately the ones known today are all toxic. On the other hand, Amantadine (Symmetrel) may be an NMDA antagonist. GDNF (glial-derived neurotrophic factor) has been in the news lately, in part because of encouraging reports at these meetings. Cheers, Joe J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks CA 91403