44 RESULTS
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 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 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 data from Leal et al. help to bring clarity to the relationships between Aβ accumulation and the AV-1451 tau signal. On a relatively small number of cognitively normal 75 years old subjects, followed over five years, those who were accumulating Aβ, ev
COMMENT We were the first to describe the association of brain Aβ deposition (both as parenchymal plaques and cerebral amyloid angiopathy, CAA) and iatrogenic Creutzfeldt-Jakob Disease (iCJD) related to dura mater grafting many years ago (Australian Communicable
COMMENT Based on the identification of full-length Aß42 and N-terminally heterogeneous Aß42 as the main Aß species in amyloid plaques isolated from patients with sporadic Alzheimer’s disease, we have postulated that Aß42 is a key player in AD pathogenesis. Indeed
COMMENT Bu et al. studied the transmission of blood-derived Aβ protein by using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates carrying the endogenous murine APP gene. In this way they made them share a blood system
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 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 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 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 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 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
