11227 RESULTS
COMMENT Clarification of the confusing terms such as Aβ, βA, APP, βAPP or AβPP will help the field if they can be standardized. But here, I would like to reiterate the key importance of another "nomenclature" problem, i.e., "Alzheimer's diseas
COMMENT This debate makes me rethink some basic issues in AD. Here I have another question. Calcium is important for brain function, no problem. But many other factors are also important such as aluminum, zinc, iron, acetylcholine, mitochondria, cAMP,or NO. Brain
COMMENT Reply to Dr. Wong by Ming Chen First, let me take this opportunity to thank Drs. Wong, Scatty and Aldoso for raising in-depth and sharp questions. In science, asking the right questions sometimes can be as important as solving them. The AD field today nee
COMMENT A very stimulating hypothesis. But, a problem is that it is all based on your findings in a single experimental paper suggesting that alpha-secretase may be a calpain. At the same time, however, there are over 50 or so proteases being also proposed today
COMMENT Reply to Dr. Aldoso by Ming Chen In the world of research, we develop hypotheses based on facts. But perhaps the most difficult job is to judge, among the numerous reports, which ones are facts and which are not. Many papers have reported that calcium ant
COMMENT To my knowledge, there are probably over a hundred of reports showing that calcium channel blockers have protective effects in old cells or animals and even in AD patients. So, whatever your theory is (though it is interesting), a rule is that one cannot
COMMENT Reply to Dr. Scatty by Ming Chen Conceptualization of Ca2+ signals in the brain as dynamic "spikes" (1-3), instead of traditionally perceived steady-state "level" changes, is essential to explain some key dilemmas that have severely ha
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
