56 RESULTS
COMMENT These interesting papers by Tsai et al. and Moolman et al. further support the idea that neuronal processes are important sites of damage during AD pathogenesis. A major question, of course, is why are processes being damaged? Is there any damage prior to
COMMENT These interesting papers by Tsai et al. and Moolman et al. further support the idea that neuronal processes are important sites of damage during AD pathogenesis. A major question, of course, is why are processes being damaged? Is there any damage prior to
COMMENT Jin et al. in the American Journal of Pathology and Magrané et al. in J Neuroscience provide further support for a critical role of intraneuronal β-amyloid accumulation. Jin et al. provide compelling data indicating that in cultured neurons with chemicall
COMMENT Mironov et al. utilize immuno-EM to localize PrPc within neurons and their processes in brain. Especially interestingly, they describe a subpopulation of neurons with markedly elevated PrPc labeling. More speculative is their interpretation that, in these
COMMENT This is an interesting study by Mathias Jucker and colleagues that attempts to define the role of extracellular versus intracellular β-amyloid in plaque formation. The pivotal experiment of the paper is their injection of embryonic brain tissue from wild-
COMMENT comments on this paper reinforce the point that the study of how mutant APP/Aβ may relate to synaptic
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 papers by Ma and Lindquist are important to AD research. Unlike most other neurodegenerative diseases, AD and prion diseases have in common that both are characterized by dementia and "extracellular" plaques. The present papers demonstrate t
COMMENT We appreciate the analysis/comments of our paper by Dean Hartley, but want to stress that this
COMMENT This is a very interesting report demonstrating that reduced synaptic Zinc decreases Aβ plaques in the well-established Tg2576 mouse model of cerebral β-amyloidosis. The study also points to an intriguing disappearance of the usual gender disparity in pla
COMMENT the instructive comments of Dr. Yankner, and would like to add (Re: his point 1) that a major reason
