42 RESULTS
COMMENT Peter was clearly one of the greatest investigators in the pantheon of Alzheimer’s researchers. I knew him as a dear friend and valued mentor since the '80s. I always valued his great balance of scientific objectivity and empathy, especially for ...
COMMENT In this study, Pandey et al. report that a γ marker (GM) allotype more susceptible to HSV-1 immune evasion mechanisms is present at higher rates in subjects with Alzheimer’s disease. The authors show that carriers homozygous for the GM 17 allotype were ...
COMMENT For anyone interested, along the lines of this excellent new study, we also recently published a paper using family-based association to identify novel AD genetic risk factors that are sex-specific, in this case actually conferring opposite risk effects ...
COMMENT Using a mutant C9ORF72 mouse model, Burberry et al. report on the impact of the gut microbiome on disease progression in ALS. They show that fecal transplant using gut microflora from mice with loss of both (-/-) alleles of C9ORF72 raised in a protective ...
COMMENT Using a new, three-dimensional bioengineered human brain model, Cairns et al. report that HSV-1 infection induces pathological changes reminiscent of those observed in Alzheimer’s disease. This study is consistent with our previous publication, which ...
COMMENT This study is a step forward to a more physiologically relevant brain organoid model. Dr. Park’s team elegantly showed a vascularized human cortical organoid (vhCO), which displays blood-brain-barrier (BBB) characteristics and vasculature-like networks in ...
COMMENT This is another groundbreaking paper from the Arlotta lab. This study tackles a fundamental challenge of brain organoid models, “heterogeneity and reproducibility.” Since generation of organoids solely depends on the self-assembly and patterning capacity ...
COMMENT Ezzat et al. show that HSV1 accumulates a multiprotein corona, which they propose enhances infectivity. The authors present data showing Aβ binds HSV1 and RSV, and that the binding induces fibrillization of the peptide. We have previously shown that Aβ ...
COMMENT This study describes a toolkit for studying neurofibrillary inclusion and Lewy body formation in an in vivo-like murine environment. Organotypic brain slice cultures have been used to study brain cells ex vivo for more than a decade. Multiple tauopathy ...
COMMENT Most AD researchers remain to be convinced that microbes are causative in AD. While we agree that the available evidence is not definitive, mounting data suggest microbes are involved in some way with AD etiology. Our own findings show Aβ is an ...
COMMENT Our study, taken together with the Readhead et al. findings, suggest a new model for amyloidogenesis in which chronic elevated viral replication may directly promote Aβ deposition in AD brain. In this model, the activation of herpes viruses serves to ...
COMMENT In response to Drs. Saido and Annaert, it is interesting to consider why there are so many more pathogenic early onset familial Alzheimer’s disease mutations in PSEN1 than in PSEN2. The numbers of mutations arising in one gene versus another depends on ...
COMMENT Investigations into possible roles for infection and associated immune response in AD etiology have a long history, but have gained increasing attention and impetus in recent years. In 2014, more than 80 publications were cited on PubMed supporting ...
COMMENT This article by Chan and colleagues offers new insights into the genetics and pathogenic effects of CD33 and TREM2 in Alzheimer’s disease (AD). CD33 was first implicated in AD in 2008, when we reported that the minor allele (G) of the rs3826656 single ...
COMMENT Twenty-five years ago, the late, great, Henry Wisniewski maintained that Alzheimer's disease (AD) was initiated by blood vessels leaking beta-amyloid into the brain. The more veteran researchers may remember Henry's colorful slide of warplanes ...
