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
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