219 RESULTS
COMMENT This work may generate a breakthrough in the field. However, I have one concern, i.e., the use of APP/PS1 mice as a model of AD. APP and PS1 contain 1 and 9 transmembrane domains, respectively. Overexpression of these proteins is likely to induce a non-sp
COMMENT Good news for the holiday season. Knock-in substitution of the proteasome subunit phosphorylation site would further confirm the exclusive PKA-proteasome connection because PKA phosphorylates a number of proteins. At the later stage when proteasome activa
COMMENT I would like to congratulate the AD researchers in the U.S. for the good news. In contrast, the total Japanese budget for dementia research is less than $50 million, although Japan is one of the most aged countries in the world. The U.S. is indeed a giant
COMMENT Please let me make the following comments on John Freyer's work, because this is very
COMMENT If you weigh 50 kg, you have approximately 60 g of IgG in your blood. Yet, immunohistochemistry of your brain parenchyma using anti-human IgG would generate essentially no immunoreactivity, indicating that only little, if any, IgG crosses the blood-brain
COMMENT In this study, the authors have attempted to associate long-range circuit dysfunction with AD pathogenesis using large-scale calcium fluorescence imaging. The imaging techniques appear quite sound, and the idea of focusing on inhibitory neurons is logical
COMMENT As a co-author, I would like to comment that BBB-permeable Gpr3-specific antagonist(s) without any
COMMENT This is a finely designed, beautiful work. A simple concern: Does replacement of the lysine residue by glutamine completely mimic acetylation in structural biology terms? At least biochemically, acetylated lysine and glutamine are quite different. saido 0
COMMENT Previously, we found that Aβ secretion from neurons is mediated by autophagy. In addition, it has been shown previously that autophagosomes contain both Aβ and the Aβ-generating enzymes (Nilsson et al., 2013; Nilsson et al., 2015). The increased levels of
COMMENT The major point made by Winton et al. was that many of the antibodies raised against Aβ also crossreact with APP and other APP fragments, not that intracellular Aβ does not exist in the transgenic mice at all. Besides, Aβ deposition, which precedes diseas
COMMENT To my knowledge, this is the first paper describing neuropathology of AD patients with Arctic mutation. 0 saido
COMMENT This is a very important study. What would the kinetics be if the authors used amyloid protofibrils and filbrils isolated from human brains? 0 saido
COMMENT The group led by Karen Ashe presents an important finding that Aβ*56, not dimers or trimers, correlate with "pathological tau" proteins and postsynaptic proteins in human brains. Everyone in the AD research field should read this paper carefully
COMMENT This is a nice update of [18F]-labeled PET ligands for amyloid imaging. 0 saido
COMMENT This work deserves a lot of attention. One thing that is unclear is the definition of tauopathy. 0 saido
