11620 RESULTS
COMMENT The study by MacAulay et al. finding that lithium inhibited GSK3 expression, which was associated with glycogen synthase activation, has me wondering what to expect in Alzheimer's disease. Allaman et al. report glycogen accumulation in AD. The fact t
COMMENT Cobbold et al. find that Menkes disease protein is enriched in the plasma membrane in the presence of excess copper, and that trafficking of MNK from the TGN to the plasma membrane is inhibited by Cdc42 and WASP. Cdc42 and N-WASP are increased in AD (Zhu
COMMENT I am optimistic about the introduction of memantine, and think it is more likely to affect a (if not the) basic trigger factor for onset of the disease. I plan to review results of long-term use of memantine in Germany, where I believe it has been used fo
COMMENT This study finding that depletion of normal prion protein prevents or reverses the clinical manifestations of Creutzfeldt-Jacob disease is interesting. Is it overexpresed as is APP in Alzheimer's disease? If the study by Kniazeva, Orman and Terranova
COMMENT This study furthers our understanding of the contribution of neuronal ApoE expression and its potential relevance to Alzheimer’s disease. This study shows that the expression of both human and mouse ApoE genes are regulated in neurons by a glia-secreted f
COMMENT The presence of HSV in brain has been correlated previously with Alzheimer's disease (Itzhaki and Dobson, 2002). The paper by Satpute-Krishnan et al. provides a clue for understanding this relationship in the form of a molecular interaction between H
COMMENT This work demonstrates the efficacy of a simple and affordable nutritive strategy to reduce the risk of cerebral atrophy thereby providing a direct service to human kind. In addition, findings from this study are of significant heuristic value for basic s
COMMENT This work is interesting, but highly speculative since the linkage between BMAA or other cycad components or cycads themselves remains tenuous, and earlier data over a decade ago to suggest that cycads or BMAA induced a progressive neurological disease in
COMMENT A requirement for intraneuronal PrP sc conversion in prion pathogenesis: What questions does this raise about the mechanism of AD pathogenesis? The recent report by John Collinge and colleagues provides important new insight into the mechanisms of pathoge
COMMENT This is a very interesting study that provides some intriguing new possibilities about cellular factors involved in prion conversion. The data are very clear and fit well with some of our own results. These findings are important not only to understand th
COMMENT This is an elegant study that shows the importance of studying further the biological role of PrPC, and the intermediates that are formed during the conversion of PrPC to PrPSc. It is interesting to compare these findings to the Alzheimer's field, wh
COMMENT Due to the genetic background used in our study, it is not surprising that the long-term degenerative effects after kainate treatment were only modest. Nevertheless, these effects were significant. Certainly, we would have preferred to work in a more suit
COMMENT These two exciting articles provide significant momentum for the field of Parkinson's disease research. The Singleton/Farrer paper cements the role of α-synuclein as a central player in the pathogenesis of PD. Their discovery of an elevated gene dosa
COMMENT In my opinion, the statement in the news release that memantine probably does not affect the underlying mechanisms causing the disease is actually counter to our current beliefs about the role of the NMDA receptor in the degeneration of vulnerable neurons
COMMENT It seems of interest that Liu and Burridge have found that EGF and PDGF stimulate tyrosine phosphorylation of Vav2 with subsequent increased activity of Cdc42 downstream from growth factor receptors. Might we expect decreased activity of Cdc42 following t
