Published in Gene Therapy Weekly, May 31st, 1999
Extracellular A(beta) amyloid deposits known as senile plaques are the distinguishing feature of AD. It once seemed clear that these plaques caused AD symptoms; indeed, several candidate AD drugs aim to dissolve them.
But evidence is accumulating that plaque formation is poorly correlated with neuronal loss and disease severity. Now De-Hua Chui of Japan's National Institute of Neuroscience and colleagues have shown in a mouse model that AD pathogenesis is already well under way by the time of plaque formation.
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