11505 RESULTS
COMMENT In the news article cited above, two important facts need clarification. First, protofibrils are fibrillar. Second, the first demonstration that protofibrils were neurotoxic was published by my group, in collaboration with Drs. Hartley, Selkoe, and others
COMMENT The final sentences of the Alzheimer Research Forum News Summary leaves the impression that the cause of the disparity is due to differences in the statistical methods used. In fact, this is not at all correct. The Rogaeva et al paper used the SAME family
COMMENT Response from Rudy Tanzi In Peter Hyslop's reply to the Alzheimer Forum News article on "A2M Revisited," he states: "The Rogaeva et al paper used the SAME family based association statistical methods as Blacker et al (ie the SDT and s-
COMMENT Thanks for summarizing the three new A2M genetics papers and our reply in Nature Genetics (May 1999) in your "News" section this month. I wanted to share my thoughts on the controversy regarding the candidacy of A2M as a genetic risk factor for
COMMENT Response from Allen Roses et al. to Tanzi Comment Below please find a short, absolute rebuttal to
COMMENT Inflammation, free radicals, and cytokines are involved in a vascular cascade producing the transformation of macrophages into foam cells between the endothelial cell layer and the basement membrane of a blood vessel leading to formation of an atheroscler
COMMENT Reply by Steven Barger Regardless of whether presenilins really are γ-secretases (for which the data seem to tipping the scales), the data seem quite clear that they are somehow involved in proteolytic processing of both APP and Notch. To me, one of the m
COMMENT Reply by E. Preddie and J. Bergmann 1. Considering what was known before, the nature of the experiments done by Wolfe and colleagues and the results obtained, it appears that the conclusion expressed by 'Ye' et al from their results is equally v
COMMENT Reply to Ratan Bhat by Rudy Tanzi: The main problem with this hypothesis is that since the time of publication of the commentary by Tuck Finch and I in Science, we now know that PS2 does not bind β- or delta-catenin (Tesco et al., J. Biol Chem., 1998). Ye
COMMENT some the mutation sites within PS1 (Tanzi and Finch in their Science comment), thereby stabilizing PS1,
COMMENT Nature, I thought it would be helpful to indicate several points about your comments regarding the role of
COMMENT As a quick comment regarding Luc Buee's summary of Dr. Lindsay Farrer's talk on the
COMMENT Dr. Lukiw does not mention that Dr. Peggy Vance reported that she replicated our significant genetic association of A2M and AD using the same A2M polymorphism (exon 18 deletion) in the same AD families (NIMH AD family set N = ~350) that we used and with t
COMMENT Dear Dr. Kosik, It was an honor that our work, presented at the Sixth International Conference on AD, was described in your briefing about presenilin-binding proteins. Similarly to your team and the identification of the catenins as possible modulators of
COMMENT This necessary study supports, once again, the idea that microglia do not affect plaque formation in mouse models unless they are "activated" by drugs or immunotherapy or replaced by fresh macrophages. Whether this applies to humans, too, remain
