25 RESULTS
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COMMENT I first heard of the idea of transposon mobilization in human brain disease from Joshua Dubnau, then at Cold Spring Harbor. Josh and his colleagues published a paper providing evidence for activation of transposable elements in association with TDP ...
COMMENT I could not think of a better person for this position, and I'm not saying that because I want a job in London! Bart De Strooper is one of the finest scientists working in the field of Alzheimer's research. My congratulations to the selection ...
COMMENT This is a heroic effort to characterize post-translational modifications of tau in the J20 human APP mouse. Two things are really notable to me: 1. The presence of the mutated human APP gene does not alter tau modification—whether that be phosphorylation, ...
COMMENT This is a nice paper, and perhaps the only issue I see is that the authors choose to use a very mild pathology model, the heterozygous P301L mouse. The effects of calpain inhibition were significant in this model, but I would argue that to compare the ...
COMMENT The assumption behind all the work with methylene blue is that inhibition of tau aggregation is going to be good for people. Some of the same arguments have been made about Aβ, but that field seems to have drifted toward the idea that it is not the ...
COMMENT One curious point about this drug, epothilone D, is that the drug is so effective at cutting down pathology, even under circumstances where there is little evidence for microtubule stabilization. If this was its mechanism of action, one might expect ...
COMMENT This is interesting from several points of view. I wonder if these studies in AD mutation carriers will be considered a better test of the amyloid hypothesis than previous or ongoing studies with amyloid antibodies. This year should see the data released ...
COMMENT The results described are surprising, and do not readily fit with the work from Mucke's group on fyn. It is also amazing how the loss of STEP corrects the behavioral impairment, without modifying the underlying pathology at all—at least at this early ...
COMMENT I was lucky enough to work with the two giants of the Alzheimer disease field in the early days (1977-1982), Robert Katzman and Robert D. Terry. What an environment that was for a young scientist! Between them, Bob and Bob knew everything there was to ...
COMMENT It is clear from the responses to our original posting that many people recognize that the mechanism by which presenilin mutations cause Alzheimer disease may be more complicated than a simple increase in Aβ production. If this is all we have achieved, I ...
COMMENT Bart De Strooper and colleagues have just published a paper on the effects of presenilin (PS) mutations on the processing of APP (and other proteins). I think this paper is extremely important, and corroborated by another manuscript currently in press. ...
COMMENT Regarding the impact of certain foods, beverages, and drugs on the development of AD, I think it is likely a situation similar to that in cancer epidemiology: A healthy lifestyle lowers risk; a bad life style enhances risk. Of course, genetic factors ...
COMMENT Tangles Come before Plaques on the Perforant Pathway The one system where transport of APP and its relationship to amyloid deposition has now been well-established is the perforant pathway. Hyman and colleagues (Hyman et al., 1986; Hyman et al., 1988) ...
COMMENT The ability to accurately identify patients with MCI who will progress to AD would be a great asset to clinical trials of drugs designed to reduce rates of progression of the disease. There is already evidence that phosphorylated tau appears in the CSF of ...
COMMENT "This paper continues the Mandelkow's fine work trying to unravel the mechanism of PHF formation by in vitro studies of structural changes that occur in tau on aggregation. Their identification of regions of tau that seem to be important for ...
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