11622 RESULTS
COMMENT López-Toledano and Shelanski report that aggregated Aβ1-42 enhances the production of new neurons, detected by BrdU labeling and βIII tubulin immunoreactivity, in hippocampal cultures in vitro. These results are at odds with some previous data (1-3), but
COMMENT It appears that this paper suggests AD to be on the same continuum as "normal" aging. However, the pattern of neuron loss in hippocampal subdivisions in AD differs from that in "normal" (nondemented) aging (e.g., West et al., 1994). 0
COMMENT When do the "earliest symptoms of Alzheimer's disease" become apparent? Evidence is mounting that cognitive deficits can be uncovered well in advance of the clinical diagnosis of AD (e.g., Kawas et al., 2003, Kawas, 2003). Similarly, we now
COMMENT The title of this paper should, apparently really be "Transgenic mice overexpressing amyloid beta protein ALONE are an incomplete----". When expression of mutated APP is combined with expression of other mutated proteins important in AD patholog
COMMENT The laboratory of David Sinclair shows an interesting feature of caloric restriction in this paper. Caloric restriction increases the levels of SIRT1, the mammalian counterpart of yeast Sir2, a nicotinamide adenosine dinucleotide-dependent histone deacety
COMMENT Is it possible that digoxin therapy may be a risk factor for the development of AD? Lin et al (1) find that digoxin treatment increases p25 in prostate cancer cells. (2) Kurup R and Kurup P report increased serum digoxin levels in AD. emaryreid 0 Involvem
COMMENT Right on. 0 Paul_Coleman
COMMENT One possible interpretation of this work is that transport of parenchymally secreted Abeta42 via ISF to CSF is suppressed by ApoE4. If so, it would be of particular interest to examine the effect of ApoE subtypes on CAA. 0 saido
COMMENT It would be interesting and probably very important to examine whether astrocytes derived from kock-in mice carrying ApoE2, E3, and E4 show any difference in Abeta degradation via exocytosis. 0 saido
COMMENT This paper should be considered a landmark in Alzheimer's research, as it laid the groundwork and provided validation for the use of members of this class of compounds as agents for non-invasive imaging of amyloid deposition in humans (Klunk et al.,
COMMENT Our unpublished observations suggest that the inhibition of NM fibrillization mediated by the oligomer-specific antibody is in fact thermodynamic and not kinetic. Therefore, we believe that the oligomeric species recognized by the oligomer-specific antibo
COMMENT This is an interesting paper that confirms and expands our published work (De Pietri Tonelli et al., 2004) on the strong repression that is exerted by the transcript leader of BACE-1 on its translation. This is a hot topic since modulation of the expressi
COMMENT The biphasic effects of the protein-remodeling chaperone Hsp104 on the yeast self-propagating prion [PSI+] phenotype have long been a puzzle. Attempts to explain the mechanism for the elimination of [PSI+] by either deletion or overexpression of Hsp104 ha
COMMENT This is a very exciting study with clever designs and elegant executions. It addresses one of the most fundamental issues in the field of neurogenesis. Adult neurogenesis, occurring in the dentate gyrus of the hippocampus and olfactory bulb in the adult b
COMMENT In search of the “β Bang” The evidence strongly favors a crucial role of the peptide Aβ in the pathogenesis of Alzheimer’s disease (AD). In vitro studies have nicely illuminated the mechanics of polymerization and fibrillization of Aβ and other proteopath
