33 RESULTS
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 ...
COMMENT In response to Dr. Schneider, who stated in his comment on the Reach2HD trial, "The trial wasn't intended as an efficacy trial and shouldn't be interpreted as one; indeed, none was found, nor should efficacy have been expected,” and Dr. ...
COMMENT While we will have to wait for the publication of the peer-reviewed paper to properly assess the results of the Reach2HD Huntington disease (HD) trial, for those interested, I have summarized below the key findings that were provided in Prana's press ...
COMMENT We would like to address the concern of Drs. Postina and Kojro, who questioned whether increased Aβ levels in the ADAM10 X Tg2576 mouse brains could be due to differences in ADAM10 expression versus effects of the ADAM10 LOAD mutations. We refer to Figure ...
COMMENT Dr. Hardy's comment that "CNVs may play less of a role in AD than they do in autism or schizophrenia" is based on recently published data from a study, which reported no overrepresentation of specific copy number variations (CNVs) in ...
COMMENT Given what Lee Goldstein, Ann McKee, and colleagues observed in the brains of blast victims and athletes who suffered severe concussions in our recent study, we need to be much more cognizant of how to protect our military and those playing violent ...
COMMENT The two new Alzheimer's GWAS reports from the NIA-ADGC (Naj et al., 2011) and European consortium (Hollingworth et al., 2011) provide further support for roles of the innate immune system, cholesterol metabolism, and protein trafficking in the ...
COMMENT To further clarify, the two mutations were present in seven out of ~1300 AD families screened. Only two unaffecteds from two different families were mutations carriers (one for each mutation). Thus, we concluded that these mutations are partially ...
COMMENT The Britshgi et al. paper nicely confirms our 2005 study (Moir et al., 2005) in which we measured titers of autoantibodies to "low molecular weight oligomeric cross-linked amyloid protein species (CAPS)," which we have long considered to be the ...
COMMENT Regarding the value of identifying all of the minor genetic risk factors for AD and the role of systems biology approaches in AD research, both are important endeavors and essential to elucidating the biological pathways involved in the etiology and ...
