Saturday, March 22, 2008

Alzheimer’s: New Protease Inhibitor Effective in Reducing Plaque Formation and Improving Memory in APP Mice

Maybe this is the treatment we’ve all been hoping for! Ninety-nine per cent of humans with Alzheimer’s have this same genetic mutation. This has not been tried in humans yet. It seems like mice have all the luck!

New research indicates that the cause of Alzheimer’s in most (99%) humans is an incorrect splicing of amyloid precursor protein (APP) by a protease named Cathepsin B (CatB). The small peptides that are formed are toxic to brain cells. These peptide particles combine to form Amyloid Beta plaques which are the hallmark of Alzheimer’s.

There is not complete agreement as to whether the resulting Amyloid Beta plaque is toxic or not.

The CatB enzyme which incorrectly splits the APP has been blocked in mice bred to have the mutation causing their Alzheimer-like disorder by the enzymes, E64d and CA074Me. This resulted in improved memory and reduced Amyloid Beta plaque.

There was no mention of deleterious side effects.

No human trials have been announced.

You can see a more complete summary of this article by going to

To see the article itself, go to the March 21 edition of the Journal of Biological Chemistry, online March 14 at

Thank you Professor Vivian Y. H. Hook and colleagues, Mark Kindy and Gregory Hook for this research.