61 RESULTS
COMMENT Alzheimer’s disease mouse modelling needs tricks, including overexpression of human genes such as APP, PSEN, or tau, and combinations of mutations in these genes, to induce relevant neuropathology. However, a complete model for AD, i.e., linking amyloid p
COMMENT Although genome-wide association studies (GWAS) have been pivotal at increasing our understanding of the genetic basis of AD, it has remained challenging to understand what the effect is of an implicated variant (i.e., which gene it affects). Novel approa
COMMENT Asher and colleagues present the conclusions from a working group convened by the National Institute on Aging to evaluate the potential risk of handling proteopathic seeds associated with neurodegenerative diseases. They provide a concise and informative
COMMENT population of African ancestry. —Rebecca Sims is a co-author of this comment. 0 EscottPriceV_288766 williamsj
COMMENT In their comment above, Colin L. Masters and Steven J. Collins rightfully pointed to a report from
COMMENT liked my work and his comments were, for me—a young scientist at the time—very encouraging and helpful.
COMMENT This is really nice work from Drs. Hur, Frost, and a team of collaborators led by Yue-Ming Li. Yue-Ming belongs to a small group of researchers who did pioneering work on the γ-secretase complex (or better yet, complexes, each having very different biolog
COMMENT This report on evolutionarily conserved gene networks mediating tau-related neurodegeneration by the group of Daniel Geschwind represents a very thorough and systematic study employing integrative co-expression network analyses in an impressive series of
COMMENT This manuscript by Daniel Felsky, Philip De Jager, and colleagues provides a new perspective on the interplay between microglial activation, amyloid-β/tau pathology, and genetic risk. The authors infer that genetic risk can lead to microglial activation,
COMMENT This paper in Cell Reports is a wake-up call for the field. It should revive interest in the γ-secretases, a field in Alzheimer’s research that got a severe blow some years ago when the failure of the semagacestat trial was announced (Doody et al., 2013).
COMMENT This failure was indeed predicted as a possible outcome of Aβ therapy (see Figure 4 of Karran et al., 2011). If Aβ is only a trigger then it will be really difficult to get the therapy right, because we do not understand when and how it triggers disease.
COMMENT The Brexit vote has shocked me, and from the reactions I hear at the Gordon Research Conference that I am attending, the Brexit is creating a lot of confusion and uncertainty among the British and to a lesser extent European scientific community. It is un
COMMENT I hope that there are "clothes for this new emperor" (see Benilova et al., 2012). To the best of my knowledge, it remains a challenge to isolate a non-covalent oligomeric structure, as every technique may affect such assemblies. I very much look
COMMENT The paper of Chen and co-authors is highly interesting, supporting the concept that γ-secretases interact with α- and β-secretases and that the enzymes are clustered in specific subdomains in the cellular membranes. It remains to be sorted out to what ext
COMMENT I wonder whether the explanation that these antibodies bind partially with APP and APP CTF, which are heavily overexpressed in these mouse models, does not explain this finding. I would recommend expanding this study to include the knock-in mice from Taka
