8 RESULTS
COMMENT There are many useful findings in this study, such as differences in gene expression involving energy metabolism and synapse pathways as indicators of healthy aging vs. “escalated” inflammation/immune responses in AD, and the presence of “AD-like” gene ex
COMMENT a C3b/C4b binding site. My comment would be to highlight the novel identification of a potential CR1 risk
COMMENT While this study demonstrated the lack of benefit of a nonselective NSAID for chronic use, targeting inflammation as a contributor to cognitive loss in the context of accumulation of amyloid remains a viable goal. The ability to slow cognitive decline wit
COMMENT California State University, Long Beach, is a co-author of this comment. atenner 0 Distribution of beta
COMMENT The rigorous quantitative data in this paper support the rationale for investigation of a less-studied group of therapeutics—those inhibiting complement-activation-dependent processes—for treatment of AD and likely for other neurodegenerative disorders, a
COMMENT This is a very interesting paper using sophisticated techniques to explore the potential role of progranulin in suppression of microglial activation. The association of genetic mutations leading to low levels of progranulin in some neurological diseases m
COMMENT The data presented by Ben Barres showed that immature astrocytes stimulate the neurons to synthesize C1q, rather than the astrocytes synthesizing C1q (as suggested in the news story above.) It will be quite interesting to determine the trigger of this ind
COMMENT There is considerable data suggesting that complement plays a role in the progression of AD, including an animal model that we published in 2004. In that study, Tg2576 animals (APP) were crossed with C1q-deficient mice to effectively eliminate activation
