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Oddo S, Caccamo A, Tran L, Lambert MP, Glabe CG, Klein WL, Laferla FM. Temporal profile of amyloid-beta (Abeta) oligomerization in an in vivo model of Alzheimer disease. A link between Abeta and tau pathology. J Biol Chem. 2006 Jan 20;281(3):1599-604. PubMed.
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Banner Research Institute
This is an important piece of evidence in the "which comes first" issue.
Inserm
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 A, Sergeant N, Champain D, Wattez A, Maurage CA, Lebert F, Pasquier F, David JP. Nonoverlapping but synergetic tau and APP pathologies in sporadic Alzheimer's disease. Neurology. 2002 Aug 13;59(3):398-407. PubMed.
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