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News for week ending 5 July 2002


A new drug to treat amyloidosis - a serious medical condition linked to Alzheimer's disease and late-onset diabetes - has been developed by University College London (UCL) scientists and the global pharmaceutical company Roche.

Trials to assess whether it will delay or prevent the development of Alzheimer's are about to begin. UCL's Professor Mark Pepys and his team have removed from the human body a naturally occurring blood protein known as SAP that is linked to the development of Alzheimer's and diabetes with promising results.

SAP is responsible for amyloidosis, a disorder in which the body's own proteins accumulate as abnormal fibres that damage organs and tissues. The ailment causes the death of 1,000 people in the United Kingdom every year. All parts of the body can be affected. Amyloid deposits localised to the brain are associated with Alzheimer's and those in the pancreas with type two diabetes.

Working with Roche, Professor Pepys developed a new drug - CPHPC - that blocks the sticking of SAP to amyloid deposits and removes it from the blood. The drug glues pairs of SAP molecules tightly together resulting in a clump of protein that is promptly removed from the liver and destroyed.

The disappearance of SAP greatly speeds up its removal from the amyloid deposits in the tissues. It is believed that CPHPC can also be used to remove SAP from amyloid deposits in the brain in patients suffering from Alzheimer's.

Nineteen patients with systemic amyloidosis have already been treated with CPHPC for nearly a year. There have been no side-effects and their condition has remained encouragingly stable.

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