11614 RESULTS
COMMENT The ability to accurately identify patients with MCI who will progress to AD would be a great asset to clinical trials of drugs designed to reduce rates of progression of the disease. There is already evidence that phosphorylated tau appears in the CSF of
COMMENT These papers provide exciting new evidence that plaque formation can occur from axonally transported APP/Aβ. Both investigations unilaterally lesioned the perforant pathway of plaque-bearing APP Swedish/PS1DE9 mice and found markedly reduced amyloid plaqu
COMMENT The article by Pfeifer et al. describes the exacerbation of cerebral hemorrhages seen in an aged APP-transgenic model following passive administration of anti-Aβ antibodies directed to amino acids 3-6. This particular transgenic mouse, called APP23, is de
COMMENT Interesting article but immunotherapy for AD has a long way to go. It may very well work in rodents but in the ageing human brain one needs a vigorous drainage route or a "solvent or a clearing agent" to go with the vaccine. This scenario is rem
COMMENT Failure of neural cholesterol dynamics is a primary pathogenic event in sporadic Alzheimer's disease In my view, the "How does it work?" scheme and "Mechanism?" question posed by Tobias Hartmann should be enhanced with the perspec
COMMENT A very interesting paper: I caution still, however, that a genetic role for UCH-L1 in Parkinson's is not yet established. 0 J.Hardy
COMMENT This provides a new insight in protein-degradation study as wellas Parkinson's Disease. It is more interesting how the varations of UCH-L1 affect both activities. 0 mori
COMMENT The recent Nature Neuroscience paper by Michael Mullan and colleagues entitled "Role of CD40 ligand in amyloidosis in transgenic Alzheimer’s mice" (see Abstract) presents exciting results showing a correlation between reduction in CD40 ligand (C
COMMENT I have to take issue on two accounts with Phil Wong's assessment of the Felbor et al. study. First, relevance to Alzheimer’s disease cannot be judged simply in terms of a protease's effect on AβPP processing. Neurodegeneration, the likely basis
COMMENT Wolozin states above that our presentations validate earlier results by Dewji and Singer, which have been criticized on the basis of both antibody specificity and suggested PS1 topology (see for example discussion by Li and Greenwald). Since this has been
COMMENT I surprised by the extent of staining by this antibody. The diffuseness argues for a more generalized neuronal problem and not necessarily apoptosis. 0 edkoo
COMMENT Surprising heterogenous phenotype from this PS1 mutation. But with only one case with the LB pathology, it is unclear whether this is a coincidence of two different processes. However, the relatively young age argues against the latter idea. 0 edkoo
COMMENT Nice correlative study but it's still the chicken and the egg. Is Abeta 42 seen intraneuronally in the neurites because the neurons are sick or the other way around? 0 edkoo
COMMENT Interesting although I am not sure IGF works through the proposed pathway, i.e through clearance of Abeta via increased albumin and transthyrethin levels. 0 edkoo
COMMENT This is a laudable effort to generate and characterize a mouse model for an FTD-related pathology. By expressing the human tau[R406W] FTD-mutant using the CaMKII-promoter, the mice express the human mutant tau protein at a rather low level (20% of endogen
