Sam Gandy on Intracellular Aβ in Alzheimer's Disease

COMMENT 45: 358-368. Abstract). Comment from Bruce Yankner, posted 15 May 2000 I would like to comment on

Brian Balin on Chlamydia Update

COMMENT reported. My comments are outlined below: The recent report by Gieffers, et al. does not address our

Peter Davies on New Study Correlates Aβ Levels to Degree of Dementia

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 wi

Bradley Hyman on New Study Correlates Aβ Levels to Degree of Dementia

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

David Teplow on Toxic Protofibrillar Aβ

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

Peter St. George-Hyslop on The A2M Deletion, Revisited

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

Rudy Tanzi on The A2M Deletion, Revisited

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-

Rudy Tanzi on The A2M Deletion, Revisited

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

Allen Roses on The A2M Deletion, Revisited

COMMENT Response from Allen Roses et al. to Tanzi Comment Below please find a short, absolute rebuttal to

Larry Sparks on Vitamin E: More Than an Antioxidant?

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

Steve Barger on In Search of γ-Secretase

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

Johanna Bergmann on In Search of γ-Secretase

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

Rudy Tanzi on In Search of γ-Secretase

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

Ratan Bhat on In Search of γ-Secretase

COMMENT some the mutation sites within PS1 (Tanzi and Finch in their Science comment), thereby stabilizing PS1,

Dennis Selkoe on In Search of γ-Secretase

COMMENT Nature, I thought it would be helpful to indicate several points about your comments regarding the role of