21 RESULTS
Go to another page:
COMMENT It seems that there are two mechanisms by which CysC may regulate cerebral β-amyloidosis. One of them we and Efrat Levy’s group described previously in Nature Genetics (Mi et al., 2007; Kaeser et al., 2007), where CysC interacts directly with Aβ fibril fo
COMMENT These are very impressive results from Virginia Lee and colleagues, and build on the previous work of the same group. The fact that synthetic material can act as a seed in wild-type mice opens a myriad of experimental approaches and avoids confounding fac
COMMENT This is an interesting manuscript. It confirms an earlier study by Wisniewski et al., 1991, which reported that invading macrophages after brain injury phagocytose amyloid while resident microglia appear not to do so. However, the question of whether a CN
COMMENT Reply to comments by Christopher Carter, Nunzio Pomara, and Gabrielle Lake We thank Drs. Carter, Pomara, and Lake for their thoughtful comments on our work. Christopher Carter asks whether our observations may be related to antibodies to β amyloid generat
COMMENT This is a very nice study by Heneka et al. Before readers reach conclusions about the nature of the amyloidogenic seed, I'd like to offer a note of caution. The authors used 0.25 mg/ml synthetic or synthetic nitrated Aβ. This is at least 50 times mor
COMMENT This is a very nice paper, and complements the prion-like spreading of Aβ (Meyer-Lühmann et al., 2006) and tau (Clavaguera et al., 2009) in transgenic mice. Strikingly, in the synuclein model, the induced synuclein pathology induces/accelerates neurologic
COMMENT This is a very carefully done and exciting study that convincingly demonstrates the existence of tau conformers ("strains") in living systems. In vivo strains have been suggested previously for tau (e.g., Clavaguera et al., 2013), synuclein (e.g
COMMENT This is a very innovative and interesting paper. Naturally, I would have expected that such a treatment would make the mice worse and not better. As the authors acknowledge, more work appears necessary to follow up on this provocative and novel finding. 0
COMMENT The possibility is raised that the spread of protein aggregates can easily be explained by the idea that cells under stress begin to form protein aggregates and thus protein aggregation can be initiated along "stressed" neural networks rather th
COMMENT These very interesting human results are in line with and predicted from the CSF analyses of APP transgenic mouse models (Maia et al., 2013; Schelle et al., 2016). 0 mathias.jucker Changes in amyloid-β and Tau in the cerebrospinal fluid of transgenic mice
COMMENT This is an important control and confirmation of the previous human transmission observations by this group. I am not surprised that Aβ in the hormone extracts seeded cerebral amyloidosis in these mice, since it is exactly what transmission studies in mou
COMMENT This nice study by Green’s group investigates what happens after elimination of microglia in the 5xFAD mouse model. The hypothesis they propose, i.e., that microglia take up Aβ and form fibrils, is interesting but not novel. Wisniewski and others came to
COMMENT This is a very informative and important paper. We should remember that there are no "mouse models of AD." Maybe we will never see any animal model that fully mimics Alzheimer’s disease (see Walker and Jucker, 2017). What we have are mouse model
COMMENT Happy birthday, astroglial inclusions! Thirty years ago, the first APP transgenic mouse model was published claiming that it develops Aβ deposits in the brain (Wirak et al., 1991). Then it turned out that these structures were not Aβ deposits, but rather
COMMENT This is terrible news! However, I think the implications the Science piece is suggesting are somewhat overblown. The Lesne/Ashe paper had far less effect on the direction of the field than the Science article claims. I think the Aβ*56 work was just one pa
Go to another page:
