Company Press Release SIBIA Neurosciences Reports Neuroprotective Potential of Neuronal Nicotinic Acetylcholine Receptor Ligands Presentation at 4th Annual Nicotine Research Conference Bryan Center, Duke University, Durham, North Carolina LA JOLLA, Calif., Nov. 4, 1998 /PRNewswire/ -- In a presentation at Duke University, scientists from SIBIA Neurosciences, Inc. (Nasdaq: SIBI - news) reported that preclinical studies of SIB-1508Y, one of the Company's proprietary neuronal nicotinic acetylcholine receptor (nAChR) agonists, and currently in Phase 2 clinical trials, has shown the ability to substantially protect neurons from degenerative changes in a rodent model of Parkinson's disease. Previous studies in rat and primate models of Parkinson's disease suggested that SIB-1508Y could offer a new approach to treatment with distinct advantages over existing Parkinson's disease therapies because of its ability to improve both cognitive and motor deficits. It is now recognized that cognitive impairment is a serious and frequent symptom in many Parkinson's patients, but no available product addresses this aspect of the disease. The animal data on neuroprotection suggests the potential for this compound to treat not only the cognitive and motor symptoms of Parkinson's disease, but to retard the degeneration of neurons, which is a hallmark of the disease process. Human Parkinson's disease is characterized by loss of the neurotransmitter dopamine in the nigrostriatal pathway, resulting in marked impairment of movement and often accompanied by deficits in affect and cognition. In the studies reported by Tadimeti Rao, Ph.D., Associate Research Director at SIBIA, SIB-1508Y offered protection against the decrease in dopamine levels in the striatum and substantia nigra in rat models of Parkinson's disease following injection of a neurotoxin, 6-OHDA, into the rat striatum. This type of lesion damages dopamine neuron terminals in the striatum and leads to a progressive degeneration of the dopamine cell bodies in the substantia nigra. The best protection was seen when SIB-1508Y was given prior to the 6-OHDA injection and followed by continued administration over a period of four weeks. In this paradigm, SIB-1508Y was able to completely protect against toxin-induced loss of dopamine in the substantia nigra and protect up to 75% of the dopamine loss in the striatum. In addition, the repeated administration of SIB-1508Y increased levels of choline acetyltransferase, a critical enzyme involved in the synthesis of acetylcholine, an important neurotransmitter for cognition. SOURCE: SIBIA Neurosciences, Inc. -- Judith Richards, London, Ontario, Canada <[log in to unmask]> ^^^ \ / \ | / Today’s Research \\ | // ...Tomorrow’s Cure \ | / \|/ ```````