11625 RESULTS
COMMENT You mentioned that transgenic mice with neurofibrillary tangles can now be created by the use of the P301L tau mutation. Neurofibrillary tangles and amyloid plaques both exist in Alzheimer's patients. Is there concrete evidence that supports the idea
COMMENT The abstract suggests that this paper emphasizes that pathological aggregates of selected proteins are a consequence of three dimensional structure. This is certainly true. However, it must be recognized that normal functioning of proteins depends heavily
COMMENT Fascinating and a clear milestone. This will most likely trigger the discovery of many more cholesterol-sensing proteins and will greatly assist the understanding of the cell biology of the lipid-protein crossroads. Tobias.Hartmann@uks.eu 0
COMMENT The concept of combining LCM samples of sub-regions of brain with array technology offers powerful promise. These authors have, furthermore, validated selected array data by quantitative RT-PCR—an obligatory addition. Authors have taken advantage of an &q
COMMENT A more exhaustive investigation of effects on gene expression than investigations limited to arrays and Q RT-PCR. Multiple effects on array profiles were detected. 0 Paul_Coleman
COMMENT Hippocampal cholinergic neurostimulating peptide precursor protein, found in this study to be reduced in the hippocampus in AD, is also known as phosphatidylethanolamine-binding protein (PEBP). Kazuki et al find (1) that 21q22.2-qter carries a gene respon
COMMENT This is a very interesting paper which confirms the observations made in a number of previous studies. The structure of the E2 region gives us a much clearer picture of the overall structure of APP. While the structure of a number of regions of the ectodo
COMMENT The exciting data presented in the Herzig et al. paper provide key insights into some of the mechanistic differences in the deposition of the Aβ peptide in brain parenchyma vs. cerebrovasculature. Hereditary cerebral hemorrhage with amyloidosis-Dutch type
COMMENT The field of complex disease genetics is in a rapid developmental mode. However, we still know frighteningly little about how gene sequence variation can affect gene function, and most genetic association studies are not designed with this in mind. Explor
COMMENT The idea of intraneuronal Aβ contributing to AD pathology certainly appears to be generating momentum, and this was evident at last month’s conference. Compelling evidence from new and established Aβ-related transgenic mouse models demonstrated that intra
COMMENT Cholesterol and Alzheimer's I would like to point Alzforum readers to see the key note by Cheryl Wellington, senior author of one of the discussed articles entitled "Deficiency of ABCA1 impairs apolipoprotein E metabolism in brain". It is f
COMMENT This paper together with their previous report (Sahara et al., 2002) implies a role for phosphorylation in tauopathy. 0 saido Assembly of tau in transgenic animals expressing P301L tau: alteration of phosphorylation and solubility.
COMMENT Beautiful and elaborate work. It would be of interest to examine in detail whether LRP-dependent clearance affects parenchymal amyloidosis or amyloid angiopathy, and whether LRP-dependent clearance is more associated with clearance through the blood-brain
COMMENT Important and interesting work, but one question. What kind of mice would be a relevant control for 3XTg mice? Sarcastically speaking, transgenic expression of BSA may accelerate tau pathology in tau transgenic mice. Thus, there remains the danger that us
COMMENT This is a powerful and noteworthy article. The authors show with strong and well-considered data that there is a link between NAD metabolism and axonal degeneration rates. Through the use of an identified mouse mutant, Wlds, which has long-lived axons, th
