80 RESULTS
COMMENT This discussion around the Shen and Kelleher paper is probably the beginning of the end of the amyloid cascade hypothesis. There is also room for the loss of function of APP, and apparently the only possible common point for a global hypothesis is the phy
COMMENT How is it that PS1(n-/-) mice have on one side severe neurodegeneration (Shen et al., 2007) and here only a subtle impairment in Schaffer LTP? 0 andre.delacourte The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathog
COMMENT This hypothesis stands also for APP. 0 andre.delacourte
COMMENT prepared Alzheimer’s mind. I welcome comments and other perspectives. Undoubtedly, Alois Alzheimer made
COMMENT The proof of concept on low-cost mice is interesting, and likely more relevant (see also El Mouedden et al., 2006). 0 andre.delacourte Reduction of Abeta levels in the Sprague Dawley rat after oral administration of the functional gamma-secretase inhibito
COMMENT EGCG also has neuroprotective effects on Alzheimer disease transgenic mouse models of amyloidosis, by increasing ADAM10 and the non-amyloidogenic pathway. 0 andre.delacourte ADAM10 activation is required for green tea (-)-epigallocatechin-3-gallate-induce
COMMENT Bravo. 0 andre.delacourte
COMMENT This paper corroborates that tauopathies can be described as a code-bar (triplet in AD, upper doublet in PSB and CBD, lower doublet in PiD, lower singulet in DM, and more to come...) that reflects the aggregation of specific sets of tau isoforms, and like
COMMENT The authors forgot to mention the role of EGCG in the activation of α-secretase, resulting in less Aβ and more sAPPα, a neurotrophic factor (Rezai-Zadeh et al., 2005). 0 andre.delacourte Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precur
COMMENT A low cost and efficient approach for drug discovery. 0 andre.delacourte
COMMENT I have some difficulty to understand this paper. There are no data of bryostatin on APP V717I mutated mice. For the other model, APP(V717I)/PS1 (A246E), the study presents data on mortality, but not on the number of amyloid plaques, nor on the secretion o
COMMENT A great discovery. I agree with John Hardy that this discovery shows, once and for all, the major role of APP dysfunction n Alzheimer disease. At first sight, the paper strongly reinforces the amyloid cascade hypothesis. However, in these familial cases,
COMMENT This paper and the one of Laird et al, same issue, are going in the same way: APP is central and Abeta is a planet (see Neve's papers). Furthermore, here we have a link between tau and APP. 0 andre.delacourte
COMMENT If BACE1 activity is increased, why don't we find more beta stub in the Alzheimer brain, even in not-yet affected brain areas? While we can agree on the hyperactivity of BACE1 in AD, this does not mean that this is a good target. 0 andre.delacourte
COMMENT In the normal human brain, there is are many beta stubs (C99) as alpha stubs. This is a fact that can be verified by a simple western blot. Why is mother nature stupid enough to make highly detrimental toxic APP-CTF in normal conditions? 0 andre.delacourt
