21 RESULTS
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COMMENT I was never a member of the Don Price lab at JHU, but as a postdoctoral fellow at the Gerontology Research Center, NIA, in Baltimore, I visited often and worked closely with members of the lab. At that time, the lab included brilliant scientists such as L
COMMENT Jucker et al., 1994; comment on Baglietto-Vargas et al., 2021). Such astrocytic inclusions occur mainly
COMMENT From en route to AAIC: This is a very cool paper overall. It’s not totally new, but I really enjoyed reading this work, and the findings makes sense to me. 0 mathias.jucker
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
COMMENT This impressive new research from the Cambridge group supports previous NMR findings of Tycko and coworkers (Lu et al., 2013; Qiang et al., 2017) of a predominant Aβ structure in a particular AD brain. Using amyloid-binding dyes such as luminescent conjug
COMMENT This is a very interesting paper that surely will stimulate discussions and further research in the field. The most convincing evidence for the suggested mechanism comes from in vitro microglia cultures using prelabeled α-synthetic synuclein. The hypothe
COMMENT comment after Jucker et al., 1992). Now, 30 years later, this study by Baglietto-Vargas and colleagues
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 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 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 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 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 Interestingly, last year, in Maia et al., we have shown that in three different APP transgenic mice, Aβ deposition seems to be ruled distinctively. In the initial stage of amyloid build-up, increased processing of APP seems more relevant, and in the secon
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 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
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