57 RESULTS
COMMENT It's amazing to have to read the "blame it on the mouse models" excuse. Those working with mice know well: mice are not patients and definitely not AD patients. They "model" one or the other aspect of AD, in most cases (over ...
COMMENT The typical feature of AD, i.e., memory loss, is irreversible. In contrast "selective memory loss" of young science writers can—fortunately—be corrected. The model reported by Rhein et al. is not the second but the "nth" with combined ...
COMMENT While appreciating the impressive FALS study by Sexena et al., I could not help frowning on the comment by P.F. Jennings: Why implicate protein tau and axonal transport? Tau-4R transgenic mice develop axonopathy leading to Wallerian degeneration and ...
COMMENT The picture is more complicated than the title of Yuan et al. would lead us to believe. Our group has generated many tau transgenic mice strains, and at least Tau-4R mice have impaired axonal transport (Spittaels et al., 1999; Künzi et al., 2002), which, ...
COMMENT The link among activated caspases, tangles, and death of neurons has been proposed based on snapshot types of analyses of patient brain, mouse brain, and cells. Experimental evidence for a causal relation was lacking, as most data did not surpass the ...
COMMENT I appreciate many, not all, of the items in the list of "hot-topics-to-be-tackled-by-fundamental-AD-research" (part 5 of Gabrielle's relentless account of the "Bar-Harbor-top"). That said, I am surprised to encounter the term ...
COMMENT A most timely topic and discussion, but one with several "open angles." One is the very recent notion that microglia (might) all come from within (Ajami et al., 2007). Moreover, microglia are activated in transgenic mouse brain long before any ...
COMMENT Besides the interesting issues already discussed at length and in depth, the data bring to mind the problem of why N-terminally directed antibodies—and particularly those against the EFRH epitope as demonstrated by Beka Solomon and coworkers—are most ...
COMMENT I agree with Charles and Beka that this is excellent work. It's actually long overdue in the AD field, which is at the same time crowded and lacking some essential experts. Nevertheless, I am more critical than my two learned friends and colleagues ...
COMMENT Lest this become the "Jurgen Gotz solo" stage, I'd like to sound my three notes: First, to thank Lon Schneider for his most enlightening dissection of the problems surrounding the Alzhemed trial. To be honest, while I had hoped for the best ...
COMMENT Not sure I can share the enthusiasm: the differences between Normal and AD are no more than a trend ... fred.vanleuven 0 ...
COMMENT I stand in awe of this painstaking, comprehensive study from Ulrike Müller and coworkers. This is probably as close as we can get to the function of APP and the amyloid peptides in vivo—and to the problem of their physiological function and pathological ...
COMMENT I proposed (ICAD-2006, Madrid) that intracerebral bleedings observed in some amyloid mouse models have more to do with their genetic background than with CAA—based on our observations of only very rare bleedings, if any, in our APP-V717I mice (in FVB/N, ...
COMMENT My initial enthusiasm, shared with commentator Tom Fagan, for this study was cooled when I tried to discover which dominant-negative mutant of GSK3β was used. The answer appears to be "none" since wild-type GSK3β was incorporated in the injected ...
COMMENT While this study helps us to understand some of the actions of tau, several questions come to mind. It is surprising that no effects are noted on spines or dendrites, while synapses are not really analysed here. The evident neurotoxicity is remarkable in ...
