17 RESULTS
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COMMENT Expression arrays in Alzheimer disease mutation-carriers: a common biochemical pathway? This paper paper ”A unique gene expression signature discriminates familial Alzheimer’s disease carriers from their wild-type siblings”, published in the October issue
COMMENT Regarding the data presented by Dennis Selkoe's group: when they isolate the oligomeric material from AD brain, they separate it by a Sephadex75 column. The material goes with the void in that column (“fraction 4”), which means that it is larger than
COMMENT It is great news that Genentech and the NIH are taking the bold initiative to start a prevention trial on the large Colombian family with a presenilin-1 mutation. One hundred presymptomatic mutation carriers will receive monthly injections with crenezumab
COMMENT Amyloid-β protein dodecamer in the brain impairs memory in the Tg2576 mouse The experience from genetic findings in the early 1990s strongly point to Aβ as the culprit in Alzheimer disease. However, we still do not understand how Aβ confers cognitive dysf
COMMENT For the first time an ELISA has been developed that is sensitive enough for detecting high-molecular-weight oligomers in human CSF, which might be an important biomarker for Alzheimer disease (AD). Soluble forms of Aβ correlate better with disease severit
COMMENT The potential of CSF α-synuclein as a biomarker for Parkinson’s disease has been investigated by Tokuda et al. The authors confirm their own previously reported findings of decreased total CSF α-synuclein in patients as compared to controls. What is novel
COMMENT I first meet Dale in 1992. He contacted me when we published the Swedish mutation, and invited me to give a lecture at Athena Neurosciences in San Francisco. Being new to the field, it was very important for me to collaborate with Dale and the researchers
COMMENT EU regulatory authorities requested in 2014 that BAN2401 be restricted from the top dose due to a few ARIA-E cases. At this time the EMA had not been exposed to many ARIA-E cases, and took a very cautious position. Patients who had been in the BAN2401 tri
COMMENT Various studies from many laboratories suggest that the most toxic forms of Aβ are not the fibrils found in plaques, but rather the soluble lower-molecular-weight species known as Aβ oligomers and protofibrils (Walsh et al., 1997; Nilsberth et al., 2001;
COMMENT The new NIA-AA Framework for Alzheimer’s disease marks a big step forward in how we are looking at this disorder and will lead to better diagnostic principles. In addition, to base the diagnosis on pathobiology instead of clinical staging will help to imp
COMMENT We remember Steve’s way of sharing his home with us during our occasional visits to San Diego. Staying with him in his house in La Jolla left warm memories for life. We gratefully remember his significant contributions to our research when we published a
COMMENT Monoclonal antibodies are very interesting as therapeutics, also for Alzheimer’s disease. They can be made highly specific for their target, which is an obvious advantage when focusing on aggregating proteins where not all forms are toxic. However, one pr
COMMENT The authors claim, based on this modeling, that aducanumab selectively reduces the secondary nucleation rate, solanezumab selectively inhibits primary nucleation, and bapineuzumab and gantenerumab act by reducing elongation of fibrils. Furthermore, the ef
COMMENT In this interesting paper, the authors demonstrate the importance of an intact meningeal lymphatic system for successful passive Aβ immunotherapy. Furthermore, gene signature data, from both a mouse AD model and AD patients, suggest a link between meninge
COMMENT This is an interesting study from the laboratories of Michel Goedert and collaborators, where the authors, Yang et al., describe molecular structures of Aβ42 filaments in human brain. The structures of Aβ42 filaments in brain have not been well-defined. H
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