11637 RESULTS
COMMENT It would certainly make sense if the medial temporal lobe is affected early and perhaps most agressively by AD, as the early clinical symptoms seems to suggest. Molecular studies also indicate that enzymatic activity is changed profoundly initially in bot
COMMENT Very good paper! 0 russot
COMMENT Can Low Calorie Intake Dramatically Improve Health and Longevity in Humans? John Phelan of UCLA and Michael Rose of UC-Irvine have developed a mathematical model that attempts to predict the relationship between caloric intake and longevity in humans, usi
COMMENT The authors place much emphasis on the role of reproduction in longevity. I can’t see what relevance reproduction has to human aging. There is no difference in longevity between humans who reproduce and those who don’t. Furthermore, the studies of the eff
COMMENT The background article by Brian Balin on the possible microbial cause of Alzheimer disease (AD) and, possibly, other degenerative diseases is intriguing and I think the microbial origin must be taken into consideration at least as a possible con-cause in
COMMENT This paper shows how critical it is to differentiate between observations that are real in the context in which they were found versus those that can be extrapolated to physiological situations. A previous study from Goldberg et al. failed to detect accum
COMMENT I disagree with an earlier comment that this study found that a greater duration of statin use
COMMENT Cowan et al., in an elegant study published in Science, showed that human embryonic stem cells (ESCs) could be used to reprogram adult somatic cell nuclei. This result had added one more possibility to the methods of alternate derivation of ESC-like cells
COMMENT 1. If unprotected dietary linoleic acid (in refined, Vitamin E-deficient vegetable oils) causes this disease (Kalmijn et al., 1997), then a decades-long history of exposure to frying and salad oils, oily cakes and dips, etc., would be highly relevant to e
COMMENT This hypothesis is old and dead. Of course hypoperfusion can increase the risk of AD, but is not shown to be strongly causative, or necessary, in amyloidosis of either the brain or other organs. Reduced blood supply to the carotid artery can, in some case
COMMENT Superb paper! I think linking this research with receptor-dependent and-independent pathways (CB1 receptors) (arachidonic acid, anadamide) will present an insightful link between lipids, cholesterol, various esters, and signal transduction via neuronal ce
COMMENT It is interesting to note that FTD occurs at a similar rate in ALS (15 percent), as ALS occurs in FTD. The overlap in sporadic cases suggests overlapping mechanisms of selective neuronal susceptibility to neurodegeneration. 0 dhg
COMMENT It is now well-appreciated that so many of the models in mice that recapitulate the mutations that cause dominant, fully penetrant neurodegeneration in humans have such mild phenotypes in mice. Here, the authors find another such mild phenotype—susceptibi
COMMENT I find this article very informative, however, it is merely educational. While I find it interesting, it is not by finding every molecular binding site and protein involved in AD pathogenesis that we will get us closer to a cure. I love molecular and cell
COMMENT I have been a CR practitioner for nearly 20 years, since I first became familiar with Dr. Wolford's work in the mid 80's. I find it interesting, if not surprising, that my biomarkers fall very much in line with those reported by Dr. Holloszy. If
