11170 RESULTS
COMMENT A possible role for abnormal mitochondrial biology in the pathogenesis of Alzheimer’s disease (AD) has been an omnipresent theme over the last decades. Regional hypometabolism, documented by positron emission tomography and abnormalities in mitochondrial
COMMENT The paper from the LaFerla lab is most interesting, and extremely well done, which I have mentioned in recent interviews to other news outlets. However, I do not think the data in this paper resolve controversies about the validity of the amyloid cascade
COMMENT This paper demostrates that Abeta forms ion channels in vivo, and that channel formation is integral to Abeta's cytotoxic properties. This is the critical extension of the in vitro work on Abeta ion channels to a cellular model. This paper shows that
COMMENT While the data presented using antibodies is consistent with results obtained in other studies, I find the data using the gamma-secretase inhibitor DAPT doubtful. Oddo, et al., write "Using an alternative approach, we show that administration of the
COMMENT These are a series of beautifully done studies, which strongly support the Aβ cascade hypothesis. However, to fully understand the potential of Aβ reduction to alter the clinical course of Alzheimer’s disease, it would be important to know whether lowerin
COMMENT There are two key features to this manuscript. The first is the obvious linkage between the presence of excess Aβ and the accumulation of early-stage phospho-tau variants. This is the first observation that reducing Aβ may slow the rate of tau filament fo
COMMENT The summary by Gabrielle Strobel was nicely done. One further aspect from Sid Gilman's talk was that although a Z score for all cognitive tests showed the treatment group better than placebo as summarized, the ADAS-Cog score for the responder immuniz
COMMENT The amyloid cascade hypothesis (ACH) does not fit with the natural and molecular history of Alzheimer's disease. Major points: The first argument against the ACH is that tau and APP pathologies always grow in parallel in the human brain (Delacourte A
COMMENT Popovic, et al. (1), find that cathepsin L is capable of truncating cystatin C which they state has a much lower affinity for cysteine proteinases than the intact inhibitor. Might this occur in the Cer mutant and could that then result in increased cathep
COMMENT 24S-hydroxycholesterol, an important oxidative cholesterol degradation product, can be used as a surrogate serum or CSF marker to monitor changes in brain cholesterol synthesis in humans and, with some restrictions, in animals. In serum samples, the conce
COMMENT The findings of decreased BDNF transport in Huntington's disease, as well as the reports by the Brady and Goldstein groups are significant, as they support the hypothesis that various neurodegenerative disorders display impaired axonal transport defe
COMMENT I agree wholeheartedly with Dr. Kjellin. I was very surprised when I reviewed the AD2000 protocol closely and realized that the study design allowed frequent and long washout periods and in the statistical design did not analyze the donepezil 5 mg and 10
COMMENT There was a 15,000-person study in Finland of carrot consumption and heart disease. No improvement was noticed. This study was about five years ago (seen in a newspaper). Have you seen any thing about using liquorice to increase memory? A concentrate was
COMMENT I believe it is the time to finally admit that Elan’s AN-1792 trial is a failure! There is no clear evidence on cognitive benefits, neither on global measures nor on neuropsychological tests; moreover, in a subset of subjects a potentially fatal complicat
COMMENT Unfortunately I couldn't make this conference but the reports are fascinating. We have argued for some time that certain plaque types are particularly dense (e.g. fibrillar and dense-core plaques) and act as microscopic 'space-forming' lesi
