44 RESULTS
COMMENT Sanjay Pimplikar is a regular commentator on Alzforum. In the current comments, I think the view promoted is too pessimistic. Although we are already in a dire predicament today because there are no effective therapies for AD, there is considerable hope o
COMMENT This commentary is very germane. A few major issues deserve further elaboration. Testing the Aβ theory of AD (rather than the “amyloid hypothesis”) still has not been accomplished. The challenges are formidable. While the “right” target may not have been
COMMENT The IMAGINE study conducted by Prana Biotechnology was a small (n=42) exploratory trial supported by a grant from the Alzheimer’s Drug Discovery Foundation to see if the novel 8-OH quinoline (PBT2) would have an effect on Aβ-amyloid burden as reported by
COMMENT These results of the Aβ CSF kinetics on 112 subjects are a major advance in quantification of the deposition and accumulation of Aβ in the AD brain. The increase in half-life from 3.8 hours to 9.4 hours over a 50-year time span is exactly the information
COMMENT The recent reports from the Aguzzi/Budka and Collinge/Brandner laboratories reminded me that we were possibly the first to describe Aβ deposition in iatrogenic CJD, in 1989 and 1996 in a 56-year-old man (Simpson et al., 1996). We thought that the concurre
COMMENT Overall, results in the CCS/SOD mice look very promising, and are consistent with other experimental data that support the concept that altering copper levels in the CNS might have some therapeutic benefits in specific conditions. This could also include
COMMENT This seems like a good systems biology approach to understanding regional vulnerability in protein-aggregating neurodegenerative diseases. The “promoters” and “protectors” selected for this initial analysis are a relatively small series, and no doubt will
COMMENT These data add to growing the evidence base that there are signals in plasma (and possibly in cellular blood elements) which are informative on the state of Aβ accumulation in the central nervous system. The technologies used in this report include the mu
COMMENT The authors have developed a microfluidics-based, solid-state impedance measure (interdigitated microelectrode [IME] sensor system) of monoclonal antibody 6E10-Aβ interactions which they claim can measure plasma Aβ levels on a scale of 0.1 pg/ml. The resu
COMMENT This is good news for the AD field in general and for the Aβ theory in particular. When Biogen announced its futility results in March, I thought that something was wrong, based on its earlier data. To read in its announcement now that “the result of the
COMMENT Apart from the topological problem (i.e., the cellular compartments in which each of the players exist: e.g., does extracellular PrP ever normally come into direct contact with cytoplasmic α-syn?), the biological relevance of these interactions remains po
COMMENT I am disappointed, but not surprised. The trial sizes were very small, and cognitive readouts are notoriously relatively insensitive. The baseline intake was very heterogeneous in terms of cognitive status (CDR ranging from 0 to 1) and the escalation of d
COMMENT Ever since the origin of Aβ was shown to be the result of proteolytic processing of the juxta-membranous and intramembranous domains of a beta-amyloid precursor protein (APP) (Kang et al., 1987), it has been apparent that this phenomenon must reflect some
COMMENT The BACE 1 inhibitors are a powerful and specific class of drugs. They were used at very high doses, aiming for 70-90 percent inhibition of APP processing (as were the γ-secretase inhibitors). With the benefit of hindsight, we should not be surprised that
COMMENT To date, I’m not convinced by any of the experimental or clinical evidence that a conventional virus underlies the pathogenesis of AD. Latent or temperate conventional viral activity may, however, play a role in the relatively common phenocopy of AD, mark
