11505 RESULTS
COMMENT I have to admit that the emphasis in calcium signaling can be a useful way to solve the old controversy over the role of calcium in AD. Apparently, experimentalists have been assuming that the time scale of calcium signaling is the same as that of the ins
COMMENT Question: Are Alzheimer's Disease and "Senile Dementia" the Same Disease? This perhaps is the most important "nomenclature" problem. AD used to refer to "pre-senile" dementia (PSD; middle age dementia). This name clearly
COMMENT Saido's team (Iwata et al.) infused labeled Aβ1-42 into rat hippocampus and found it was metabolized with a half-life of 39 minutes. They tried many classes of peptide inhibitors and found that neprilysin type were the only ones that prevented the br
COMMENT I agree that it would be useful to accept a uniform nomenclature. For instance literature searches in Pub med would be more efficient. Sloppiness is probably the most important reason for the current situation and the forum is a good place to discuss the
COMMENT [I would like to note] that back in [August] 2000, we published a paper in Neurobiology of Disease (Refolo et al., 2000) demonstrating for the first time that cholesterol metabolism accelerates β-amyloid accumulation in a transgenic mouse model of AD. We
COMMENT Yes, at least some consensus would be appreciated, especially for people new to this field. For example, at the recent Neuroscience meeting in New Orleans, people were hedging on the latter case (presenilin-1 or γ-secretase?) even to the extent of questio
COMMENT There is nothing that upsets me faster than scientists using inappropriate and imprecise terminology and nomenclature. With respect to the Alzheimer's disease lexicon, the WHO and the International Nomenclature Committee on Amyloidosis have ALREADY d
COMMENT Coupling of cellular prion proteins to Fyn is a real surprise, but maybe it shouldn't be. Fyn keeps popping up. Shirazi and Wood showed that tangle-bearing neurons in AD have a hefty overload of Fyn. Gloria Lee showed Fyn and tau co-localize. Gail Jo
COMMENT The part of this report referring to Davies's earlier work (with Lu) on Pin1 and tau (Lu et al) is completely misleading. I quote: "Davies and colleagues previously have shown that Pin1 is present in Alzheimer's tangles, and that its bindin
COMMENT the instructive comments of Dr. Yankner, and would like to add (Re: his point 1) that a major reason
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 45: 358-368. Abstract). Comment from Bruce Yankner, posted 15 May 2000 I would like to comment on
COMMENT reported. My comments are outlined below: The recent report by Gieffers, et al. does not address our
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
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
