11617 RESULTS
COMMENT These are really exciting results, and we are likely looking at a historical crucial manuscript providing the proof-of-principle that a cure for AD is possible, and definitively establishing the amyloid hypothesis for AD. 0 Bart.DeStrooper
COMMENT Gazit and his student, Meital Reches, have achieved something others have tried for many years, from a complete different route. This again demonstrates the crucial aspect of the curiosity-driven research that can eventually alter a concept or start up ne
COMMENT This is most welcome news! One hopes that this journal can spawn a thorough registry of negative clinical trial results so that investigators can refocus their efforts on more promising targets of disease pathogenesis. Whatever its eventual focus, the Jou
COMMENT Interesting but was already suggested in Neuroscience. andre.delacourte 0 Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100.
COMMENT Neurofibrillary tangles consist of tau protein that has forsaken its role as a stabilizer of microtubules to polymerize into abnormal fibrils within neurons. Preclinical and clinical evidence leaves little doubt that abnormal tau polymerization is injurio
COMMENT An interesting observation emanating from the studies of Noble et al. is that the double-transgenic mice overexpressing p25 and mutant tau show an increase in the active form of GSK3β while total GSK3β levels remain unaltered. Although the GSK3β kinase ac
COMMENT Tau aggregation is a central issue for understanding tauopathies, including AD. Crossbreeding CDK5-activator p25 transgenics with P301L transgenics resulted in hyperphosphorylation of human tau and induced tau aggregation in neurons. The correlation betwe
COMMENT It was with surprise that I read these results about the role of LiCl in GSK3 inhibition that confirmed and extended our results (reported in Neuroscience Letters, 2002). Recent technological advances in methodology that uses RNAi clearly showed that GSK3
COMMENT One of the critical questions in β-amyloid immunotherapy is whether depletion of the amyloid plaques is accompanied by improvement in behavioral/neurophysiological impairments and in a reduction in the nerve cell death of Alzheimer’s disease. In other wor
COMMENT Phosphorylation of proteins is known to be associated with neurodegeneration, but the causal relationship between phosphorylation and neurodegeneration is unclear. Two articles by the laboratories of Harry Orr and Huda Zoghbi in the current Neuron and Cel
COMMENT The papers by Chen et al., 2003 and Emamian et al., 2003 offer compelling and complementary evidence for the significance of a single phosphorylation event—serine 776 of ataxin-1—on the pathogenesis of the polyglutamine-induced neurodegenerative disease s
COMMENT This paper is very relevant to our work and that of others. It begins to bring together the roles of tau dysregulation and aberrant phosphorylation in a mammalian model. It further demonstrates the role for tau hyperphosphorylation in accelerating NFT pat
COMMENT This paper shows that immunization with Aβ may slow the progression of Alzheimer’s disease, but does not restore cognitive function. These results contrast with studies of immunoneutralization of Aβ in AβPP-transgenic mice, which demonstrate reversal of m
COMMENT I have never understood why GSK3α was neglected in studies of Alzheimer's neurodegeneration for the past two decades. The enzyme has over 90 percent homology with GSK3β, is also inhibited by lithium, and both isoforms are abundant in brain. The possi
COMMENT During the last 10 years, much evidence has been reported in support of the amyloid hypothesis for the progression of AD. However, the key finding of whether inhibitors of Aβ amyloidogenesis would lead to a cognitive improvement was missing. In this very
