Scientists at the UK's University of St Andrews have developed compounds capable of blocking a nerve cell interaction known to lead to the symptoms of Alzheimer's disease and have shown that it is possible to reverse some of the signs associated with this neurodegenerative disorder.
The brain malfunction in AD patients is caused by deposits of amyloid beta protein, which inflicts damage by interacting with an enzyme called amyloid beta alcohol dehydrogenase (ABAD), a recently-discovered target in AD research. An Anglo-American team led by Frank Gunn-Moore studied the structure of ABAD and produced an inhibitor that can prevent amyloid attaching to it in a living model. "We have shown that it is possible to reverse some of the signs associated with AD," noted Dr Gunn-Moore. The news comes after last week's announcement by Samaritan that its drug Caprospinol (SP-233) cuts the number of beta amyloid plaques in models of AD, with complete memory recovery for treated animals (Marketletter July 13).
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