Published in:
01-02-2011 | Editorial
Tau pathology in children and young adults: can you still be unconditionally baptist?
Author:
Charles Duyckaerts
Published in:
Acta Neuropathologica
|
Issue 2/2011
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Excerpt
The lesions of Alzheimer Disease (AD) pathology, senile plaques and neurofibrillary tangles, are made of an accumulation of Aβ 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 Aβ was the initiator and tau, the follower. The “cascade hypothesis” according to which the trigger is Aβ accumulation [
8] was further supported by the finding that mutations of
MAPT, the tau gene, cause a pure tauopathy without Aβ accumulation [
9,
13]. …