27 RESULTS
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COMMENT The paper by Ising et al. is a very important contribution to defining the deleterious roles of microglial activation in promoting tau pathology. It adds to these authors’ prior data finding analogous influences of inflammasomes upon amyloid pathology in ...
COMMENT One weakness of epidemiological evidence is the association does not permit cause-effect relationships to be determined. There are physiological reasons some individuals elect to take NSAIDs and others do not. Instead of the NSAIDs themselves providing ...
COMMENT This is certainly disappointing. Crenezumab was my initial choice to be an effective antibody. It had two unique features making it distinct from other antibodies against amyloid in clinic testing. First, as an IgG4 variant, it had limited interactions ...
COMMENT The above conversation neglects to consider the impact of microglial activation on other pathologies, particularly tau deposition. Over 15 years ago, lipopolysaccharide injected intracranially was demonstrated to rapidly clear some forms of amyloid ...
COMMENT I think the observations that increasing TGFβ shortens lifespan and blocking TGFβ increases lifespan (assuming the drug does what it is intended to do) are important. ALS has no effective treatments. The paper reinforces the idea that microglial ...
COMMENT One concern I have with the bapineuzumab trials is that the doses had to be reduced due to the issue of vasogenic edema (ARIA-E). Although it is uncertain if this is related to the microhemorrhage found in the mouse models and the active vaccine trial, if ...
COMMENT The data presented in this paper show the most rapid removal of Aβ of any systemically applied therapy. They hold great promise for testing the amyloid hypothesis, and possibly for application in secondary prevention trials of asymptomatic patients where ...
COMMENT Here is my quick reaction to these intriguing papers, without the benefit of having had time to fully consider their impact. BACE1 is an intracellular target. This raises a level of challenge for antibody action beyond the blood-brain barrier, though it ...
COMMENT This is state-of-the-art technology measuring sizable cohorts of human samples and fairly conclusively answers a question that was controversial in the literature regarding the levels of anti-Aβ antibodies in AD versus control samples. My take-home ...
COMMENT This is a very important paper that was performed very professionally and addresses a critically important question regarding immunotherapy for Alzheimer disease. The observation that centrally administered antibodies have different characteristics than ...
COMMENT This paper describes a mechanism by which macrophages may participate in the development of congophilic amyloid angiopathy. The results are consistent with Aβ-engorged macrophages being unable to transit across the endothelial cell barrier, ultimately ...
COMMENT The manuscript by Schroeter et al. demonstrates that even in middle-aged mice, anti-Aβ immunotherapy can cause increased vascular leakage. Importantly, the Schroeter et al. report indicates that high dose antibody treatment can prevent the formation of ...
COMMENT This is a very timely and important paper that supports a more sophisticated view of the role of inflammation in amyloid deposition. Ten years ago, most in the Alzheimer research community believed that inflammation was part of the pathogenic mechanism in ...
COMMENT I have a couple of quick points to make. First, Michael Agadjanyan is a brilliant immunologist. He and Dave Cribbs have been leaders in the development of safer and effective active immunization protocols against Aβ, both in this manuscript and others. ...
COMMENT I have a couple of thoughts. First, there is no good evidence, other than correlative, that age-related memory declines in canines are secondary to amyloid accumulation. Rats and mice show age-associated loss of memory without amyloid accumulation. ...
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