Paul Aisen on Safety Concerns Halt ADAPT Trial
COMMENT Without seeing the data, I cannot comment on the decision to halt ADAPT. But note that in 2000,
11631 RESULTS
COMMENT Without seeing the data, I cannot comment on the decision to halt ADAPT. But note that in 2000,
COMMENT for your comments on our paper which describes a possible link between leptin and AD-related pathways.
COMMENT Reply by Charlie Glabe With regard to the question of our recent work and the channel hypothesis, our work supports the general tenet of the channel hypothesis in that amyloid oligomers permeabilize membranes. The details are different because we do not o
COMMENT This news summary states that Dr. Glabe's work weakens the channel hypothesis. On the contrary, I think his work is completely consistent with and supports the basic premise of the model, i.e., membrane disruption and loss of ion homeostasis. Where h
COMMENT Many researchers and clinicians agree that there is great value in developing imaging technologies for the quantitation of amyloid deposition in human brain. Potential benefits of this effort include improved diagnosis of AD, particularly in early and con
COMMENT The experiments presented by the Lazano group are solid because the authors have been careful to cover as many bases as they can to test their major hypothesis: that BAG5 is a natural inhibitor of parkin function. But as well as being careful science, the
COMMENT Leaping on Leptin: What’s the Skinny? The work by Fewlass and colleagues [1] provides an impressive array of data suggesting that leptin hormone homeostasis and/or dysregulation bears upon the metabolism of amyloid-β (Aβ). Although not confirmed by neurop
COMMENT This is a timely report, since it has been recently shown that FMRP is definitely associated with brain polyribosomes (see Stefani et al., 2004 and Khandjian et al., 2004). The data reported by Weiler et al. show that synaptoneurosomes from the Fragile X
COMMENT With reference to Alzheimer disease and memory mechanisms, this paper identifies 600 phosphorylation sites on synapses. Synapse formation and destruction are critical aspects of memory. Further, phosphorylation is a critical part of synaptic plasticity, a
COMMENT This is a good paper, suggesting a new focus, and I only have one question. Is it clearance of soluble Aβ or aggregated Aβ? 0 jparodi
COMMENT I read the paper and enjoyed the new view presented by these authors.... However, I do not understand the definition of "soluble oligomer." Is this a protofibrillar solution? Are amylospheroids in the sample? Or is there just monomer in the solu
COMMENT I have always wondered if much higher than normal HDL could have an effect. I only know of one person who has such a condition and that person has now developed dementia problems. 0 ejshaner
COMMENT This is a thorough and fascinating report by Nikolas Tezapsidis that shows a clear association between leptin and Aβ levels, at least when leptin is introduced into a variety of experimental systems, including the Tg2576 mouse model. It will be important
COMMENT This paper adds to an increasing body of literature indicating that chaperones modulate neurodegenerative disease. 0 bwolozin
COMMENT This provides evidence of yet another cholesterol-related protein that might be associated with Alzheimer disease. 0 bwolozin