New insight into the pathogenesis of Alzheimer's disease has encouraged Swiss pharmaceutical major Roche to collaborate with UK researchers on a new approach to treating the disorder. The work centers on the discovery of a blood protein, called serum amyloid P, which may play a role in the formation of the amyloid plaques which are characteristic of AD. The research has been published in the Proceedings of the National Academy of Sciences (May 9).
Mark Pepys and colleagues from Hammersmith Hospital in London have found that SAP binds to the amyloid deposits in the brain and exerts a protective effect against enzymatic and immunological degradation. In in vitro studies, they have demonstrated that SAP blockers can prevent binding of the protein and also displace it from plaques, opening the way for their breakdown.
If this is confirmed, it is a striking discovery. Most researchers hold the view that once amyloid is laid down it is impossible to remove it, but Dr Pepys believes the plaques are in a state of dynamic turnover. Thus, interrupting the process actually offers the potential of reversing the progression of dementia. While drugs to manipulate this are still years away, in the near-term the researchers hope to develop a strain of mice which lack the gene for SAP. If their theory is correct, amyloid deposits will not build up in these mice, and it will also allow them to test what other systems may be affected by blocking SAP.
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