Researchers in the US have isolated a toxin from the venomous cone snail, which lives in the sea.1 The nerve poison latches onto receptors in the brain and its chemical structure could be used to design new drugs that interact with these receptors and treat psychiatric and brain diseases, such as Parkinson's disease, Alzheimer's disease, depression, and nicotine addiction.
Michael McIntosh of the University of Utah first came to prominence in 1979 when he discovered a toxin from the Conus magus, the magician's cone sea snail. This was developed into the cancer and AIDS painkiller Prialt, which was approved in the US in 2004 and in Europe in July 2006.
McIntosh and colleagues from the University of California, San Diego, and the Korea Research Institute of Bioscience and Biotechnology recently studied the snail Conus omaria, which lives in the Pacific and Indian Oceans and eats other snails, and discovered the new toxin α-conotoxin Om1A. McIntosh says the OmIA toxin will be useful in designing new medicines because the molecule fits like a key into the nicotinic acetylcholine receptor 'lock' found on nerve cells in the brain and the rest of the nervous system. 'Those are the same types of receptors you activate if you smoke a cigarette', he explains, 'but they have more important natural uses whether you smoke or not'.
Different forms or subtypes of nicotinic receptors control the release of different neurotransmitters - molecules that act as chemical signals in the human nervous system. Controlling these receptors selectively might one day help in designing drugs that control the tremors associated with Parkinson's disease, for instance, which are caused by too little of the neurotransmitter dopamine being released.
McIntosh expects it will be between 10 and 20 years before this new compound is developed into a marketable drug. After all, it took almost a quarter of a century to develop Prialt from first discovery into approved pharmaceutical.
Medicines that block other nicotinic receptors could be used to help people stop smoking cigarettes. Other conotoxin-based drugs could improve the release of neurotransmitters involved in memory and so ameliorate symptoms in Alzheimer's disease.
McIntosh confesses that the toxin itself will probably not be used as a drug because it blocks rather than stimulates nicotinic receptors. However, because the molecule binds to some types and not others, it could be used in identifying the shape and structure of these receptors. This information would make it easier for chemists to design new drugs to fit those receptors and trigger them to release desired neurotransmitters.
M. McIntosh et al, J. Biol. Chem., 2006, 281, 24678.
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