This is an important piece of evidence in the "which comes first" issue.

View all comments by Paul Coleman

There is no doubt that the link between tau and Abeta pathology is the key to understand AD. Looking if Abeta oligomers are inducing tau pathology is certainly most interesting. However, the authors of this paper as well as many "oligomer" believers have to answer this question: if these species are so toxic, and because clinical impairment of familial AD starts around the forth decade, do they think that during 40 years with APP dysfunction there is no formation of oligomers? If so, why does dementia caused by this very toxic species start only at the age of 40 in general? PS: Of course, I understand that this paper is dealing only with FAD, since the first sentence of this abstract is not relevant for sporadic AD.

References:
Delacourte, Neurology, 2002.

View all comments by Andre Delacourte