59 RESULTS
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 nuc
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 b
COMMENT In response to Dr. Schneider, who stated in his comment on the Reach2HD trial, "The trial
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
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 contac
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 etiolo
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 penetran
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 patho
COMMENT In the field of genetics, it is a rare and precious opportunity that we are afforded as scientists, when we can assess the effects of multiple mutations in multiple genes leading to common clinical and pathological disease phenotypes. We have this privile
COMMENT Update: With regard to my earlier comment on the SORL1-AD genetic association study by Rogaeva et
COMMENT This new study showing association of SORL1 with late-onset Alzheimer disease (LOAD) provides further support for a role of this gene in AD, confirming earlier studies by Lah, Small, Gandy, Masters, and others implicating SORL1 in AD pathogenesis. The nov
COMMENT We first described the PSEN1-R269H mutation in a single case of early onset AD (Gomez-Isla et al., 1997). There, the R269H PS1 mutation was associated with higher amounts of total cerebral Aβ and Aβ x-42, and increased NFT counts. Like the PSEN2 N141I mut
