52 RESULTS
COMMENT This is a well-reasoned analysis of the protein-spread hypothesis that should be studied by every AD investigator. Some important take-away messages: “The molecular mechanisms of PrP proliferation and neurotoxicity in ‘classical’ prion diseases are not ...
COMMENT Left unexplored in this otherwise inclusive analysis of the pathogenesis of AD is any discussion of the factors that initiate the various pathogenic processes that precede and lead to the accumulations of “toxic” amyloid and tau. A case can be made for ...
COMMENT There are a number of puzzling aspects of the manuscript from the Yankner lab and the comments provided by different reviewers. The most remarkable is the lack of any citation, either by the authors of the manuscript, or any of the commentators, of ...
COMMENT I agree that all the studies described in this new initiative should be supported, despite the negative results of recent anti-amyloid clinical trials that have focused on treating individuals with symptomatic dementia. It is certainly a good idea to ...
COMMENT Questions for thought leaders: Why are we putting most of the diagnostic and treatment dollars into the amyloid basket? Isn’t it generally acknowledged that amyloid deposits are a feature of the late stages of the disease? Do we really know which forms of ...
COMMENT This paper explores the use of two low-molecular-weight compounds that can block the interactions between Aβ peptides and RAGE. One high-affinity RAGE-specific blocker can bind to RAGE on luminal surfaces of brain vessels, but the other, called FPS-ZM1, ...
COMMENT This paper deals with the question of whether small blood vessel damage is a primary factor in the pathogenesis of AD, an idea advanced years ago that has since been eclipsed by the deluge of experimental data that incriminates amyloid aggregates as the ...
COMMENT Alzheimer’s dementia is a human problem that is still woefully under-supported and underinvestigated. But investing so heavily in multibillion-dollar clinical trials based on current knowledge should not be the only solution. The costs, societal and ...
COMMENT How can mice with so many genetic defects possibly reflect the pathophysiology of the earliest, asymptomatic, pre-amyloid accumulation stages of human AD? If this question cannot be answered positively and persuasively, it matters little what form of APP ...
COMMENT When brain scans to detect protein deposits in the brains of Alzheimer’s patients were first introduced in 2002 they were, and remain, the only reliable way to detect amyloid plaques in living people. But the FDA was wise to restrict their use to ...
COMMENT Few would disagree with the view that knowing the cause of a disease greatly enhances the prospect of designing effective therapies. Antibiotics for specific infectious agents are one obvious example. Recognizing the presence of dementia is rarely a ...
COMMENT One can only applaud the courage and commitment of the investigators involved in this study. It is surely a wise move to follow people with dominant mutations who are clearly at risk for clinical AD, and the markers to be studied are probably the best ...
COMMENT Two things about this study puzzle me. I don’t understand why the uptake of Aβ peptides by macrophages in culture necessarily mimics the development of plaques in the brains of AD patients, or why it is even a good model system. The claim that ...
COMMENT Some thoughts on this interesting proposal: This article raises important questions regarding our ability to monitor the pathogenesis of AD. How can we detect the earliest changes in the human brain that will eventually lead to clinical dementia? Where do ...
COMMENT It seems clear that modern scanning methods have essentially replaced the tissue diagnostic criteria of the autopsy in defining the anatomical changes that accompany clinical Alzheimer's dementia. It also appears, at least to an outsider, that what ...
