45 RESULTS
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 ...
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 Zhang and colleagues suggest that late-onset Alzheimer’s disease is oligogenic (~100 genes), whereas our earlier publications suggest that LOAD is polygenic (thousands of genes, Escott-Price et al., 2015). There is no fundamental reason why Alzheimer’s ...
COMMENT In their comment above, Colin L. Masters and Steven J. Collins rightfully pointed to a report from 1996 of what most likely is the first case of Aβ transmission after a graft of human dura mater material (Simpson et al., 1996). We want to acknowledge here ...
COMMENT With Peter, the field loses a pioneer and a charismatic and inspiring leader. Personally, it feels like losing a friend. His work was fundamental to the acetylcholine hypothesis and the first drugs for Alzheimer’s disease. In later years, he focused on ...
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 ...
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 ...
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 ...
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 ...
COMMENT MicroRNA expression profiling studies of the AD brain have yielded invaluable information about microRNAs whose expression consistently differs between healthy and diseased CNS. These findings not only shed light on regulatory mechanisms possibly ...
