9311 RESULTS
COMMENT From various studies examining the toxicity of Aβ, it is clear that random coil monomeric Aβ is not toxic whereas oligomeric aggregates (protofibrils, ADDLs or fibrils) are. Thus the critical issue with respect to Aβ toxicity is its aggregation state. An ...
COMMENT The idea that intracellular Aβ injures neurons and causes dementia prior to the formation of extracellular deposits is not obviously reconcilable with other evidence indicating that "full-blown" structural pathology precedes dementia (Crystal H, ...
COMMENT This letter is in response to the recent article in Journal of Clinical Microbiology (38[2]:881-882, 2000) entitled "Failure to detect Chlamydia pneumoniae in brain sections of Alzheimer's Disease Patients" by Gieffers et al. Since we were ...
COMMENT The study shows that both the 40 and 42 amino acid amyloid peptides were elevated early in Alzheimer's disease and that levels of both peptides are strongly correlated with cognitive decline. These are novel and important observations. However, as ...
COMMENT This is an interesting study that does, indeed, push ahead in some ways the type of correlational studies that have been going on for years. The power of the study is the large number of subjects and the use of ELISA technology to quantitate Aß. There has ...
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 the comments made by Rudy Tanzi. It is followed by a fairly detailed commentary on each point, including copies of relevant dated correspondence that clarify ...
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 ...
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 ...
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 ...
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). ...
COMMENT Question from Ratan Bhat There have been suggestions that an increase in beta-catenin could mask some the mutation sites within PS1 (Tanzi and Finch in their Science comment), thereby stabilizing PS1, decreasing γ-secretase activity and subsequently β ...
