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Springer-Verlag 2011 The lesions of Alzheimer Disease (AD) pathology, senile plaques and neurofibrillary tangles, are made of an accumulation of Ab peptide in the extracellular space and of tau protein in the neurons. The discovery that a mutation of the amyloid precursor protein (APP) gene was able to induce AD, naturally led to conclude that Ab was the initiator and tau, the follower. The ‘‘cascade hypothesis’’ according to which the trigger is Ab accumulation [8] was further sup

Tau pathology in children and young adults: can you still be unconditionally baptist?