11505 RESULTS
COMMENT As is often the case with transgenic rodent models of human neurodegenerative diseases, a single strain of genetically engineered animals rarely recapitulates the entire pathological spectrum associated with the human phenotype. The same is true for the i
COMMENT This paper describes an extremely important and exciting result that clearly demonstrates for the first time that both human tau as well as the Drosophila homolog of GSK3b, (a kinase implicated in abnormal tau phosphorylation) are essential for neurofibri
COMMENT Reply from Inez Vincent Definitely, this would be worthwhile. Recent data supports the idea that phosphorylation of APP at the thr668 site alters its interaction with Fe65, and beta-amyloid production (Ando, 2001). What needs to be determined is which kin
COMMENT This is a beautiful paper that follows a large body of excellent work from these investigators. However, no data is presented as to how the disruption of the interaction between SAP and amyloid fibrils by their drug candidate affects the fate of the amylo
COMMENT I cannot accept the statement in the introduction that the association between elevated homocysteine levels and Alzheimer's disease is weak. An odds ratio of 4.5 was found for histopathologically-confirmed AD in our case-control study (Clarke et al,
COMMENT This is a well-written and very exciting paper. Born and colleagues eloquently report on the intranasal administration in human subjects of three peptides, melanocortin (4-10), vasopressin and insulin, demonstrating direct access to the cerebrospinal flui
COMMENT I was not surprised by this paper. Though the abstract says, "This role in fate specification was unexpected," we have already indicated (Brannen & Sugaya, 2000) that astrocytes may contribute to cell fate regulation in human neural stem cel
COMMENT After 10 years of accumulating data that implicated zinc and copper in the corruption of β-amyloid, the theory that zinc causes amyloid pathology has rapidly become validated. The current study from Dr Koh's lab gives added impetus to the growing bas
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 This paper provides long-awaited in vivo evidence that zinc plays a major role in cortical amyloid deposition. These workers show that mice deficient in ZnT3, a transporter required for zinc transport into synaptic vesicles, leads to markedly lowered conc
COMMENT The involvement of an inflammatory component in AD has been amply documented over the last decade and has led to a number of clinical trials of anti-inflammatory agents. The epidemiological data clearly demonstrate that a subset of NSAIDs are effective in
COMMENT Among the most difficult problems for those interested in understanding the structural biology of amyloidoses are how to determine the complete three-dimensional structure of amyloid fibrils and to monitor the protein folding events leading to formation o
COMMENT Evidence for a link between apoptotic markers and HSV encephalitis is clearly a major step towards unraveling the mechanism by which HSV causes neurons and other brain cells to die. I'm not sure how it was determined that the apoptotic cells were act
COMMENT The nimesulide trial represents another failure in applying the epidemiological evidence of NSAIDs protecting against AD toward successful treatment. There are some simple explanations for this failure. First of all, a mismatch exists between the NSAIDs u
COMMENT This is the third small report of a trial of a non-steroidal anti-inflammatory drug (NSAID) for the treatment of AD. As in each prior study, the intent was to test the efficacy of an NSAID (in this instance, the COX-2 preferential agent nimesulide) for im
