57 RESULTS
COMMENT One could fill many more pages with discussions on this topic, pro and con the different theses. It strikes me that arguments / convictions / hypotheses / beliefs that I read here over the last weeks all appeared too familiar. AD-researchers seem to ...
COMMENT The first sentence of Pat McCaffrey's news summary is both enlightening and puzzling: "Alzheimer disease rages in the brain long before plaques form...." It was not that long ago that the century-old adage "amyloid in plaques is the ...
COMMENT Activation of α-secretase activity to increase non-amyloidogenic processing of APP is definitely one of the hottest topics among the current experimental approaches in AD. Undoubtedly, it also constitutes a major challenge (but are there minor ones in AD? ...
COMMENT One should not forget my favorite natural anti-oxidant, currently being tested in a limited pre-clinical phase in my "red wine project" ... My personal, although statistically irrelevant, approach is scientifically underscored with hard ...
COMMENT It is very satisfying to see a totally independent confirmation of our work, especially when important conclusions are directly attached to it. After we identified PS1 as essential for γ-secretase activity (De Strooper et al., 1998) we all hoped it would ...
COMMENT The results reported by Raphaelle Pardossi-Piquard and colleagues are most interesting and also provocative. The implication is that the amyloid peptides (any or all) exert a physiologic function (which I have not seen demonstrated), and that this ...
COMMENT Both Cell papers extend the cascades up- and downstream of GSK-3β considerably by providing molecular links from growth-factor signalling and cell adhesion to microtubule dynamics and axon organization—all most essential processes in evolution in " ...
COMMENT The identity of substrates of γ-secretase is becoming more and more interesting—although the wealth of putative candidate substrates is also becoming somewhat disturbing. Scrutinizing all of them to define the exact physiological role (if any) of the ...
COMMENT This excellent paper draws renewed attention to the (other) central problem in neurodegeneration in general and AD in particular: How does the tau pathology originate? This essentially boils down to the question of what is the initial kinase, i.e., the ...
COMMENT That PS1 keeps a most amazing profile is no longer a surprise, but the results reported now by J. Singer and colleagues will certainly invigorate the debate about the "firmness" of some concepts. First, let's recall the data of this same ...
COMMENT This is exactly what we predicted (Dewachter and Van Leuven, 2002) or, as the Americans would put it, "what the doctor ordered…" The overall message of this study is loud and clear: BACE is hereby proven to be the favorite target for drug-makers ...
COMMENT Re: Causes of premature death in APP transgenic mice…and how to alleviate them. The premature death of APP Tg mice is a practical problem—as anyone knows who has talked to biotech or pharma companies about licensing a strain of mice that lives ...
COMMENT Aggregation of protein tau is strongly catalysed by polyanions, including mRNA but also polyglutamate and heparin and glycosaminoglycans... That is in vitro! In vivo, in the cytosol or axon, protein tau probably sees so much polyanions that one wonders ...
COMMENT This is an excellent study on a novel C. elegans model for FTDP-17 tauopathies, with an eventual bearing on AD. The worms were humanized for tau and overexpress either wild-type or mutant tau in isoform ¡§4R1N,¡¨ i.e., containing the four microtubule ...
COMMENT The header rather than the data come as a surprise, given the fact that APP(V717I) transgenic mice display a robust defect in LTP as well as in cognition (water maze) as early as age three to four months. This is in essence the most "early" ...
