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  1. As a further comment to this article I want to be perfectly clear that this study helps support the work that many of us in the infection arena of Alzheimer’s research have been looking at for almost three decades. I cannot even begin to address the enormity of this work by so many investigators around the globe, although if one searches in PubMed, most of these articles are readily obtainable. However, there are a few points that I would like to address. Specifically, with regard to looking in human AD brain tissues which is now proposed as a follow-up study to the current Kumar et al. report, we reported on finding Chlamydia pneumoniae in AD brains in 1998, Ruth Itzhaki reported on HSV1 in human brains in 1991, and Judith Miklossy reported on Borrelia species in AD brains in 1993. These are just three reports on infectious agents in human AD brains out of many, many more in the literature. Furthermore, from my lab we have demonstrated that Chlamydia pneumoniae, a respiratory intracellular organism, inoculated through a normal route (i.e., intranasally) into normal non-transgenic mice actually resulted in amyloid plaques in the brain (Little et al., 20042014). These studies already demonstrated that amyloid could be a consequence of infection entering the CNS and we believe this will result in pathological accumulations, especially in human brains. Itzhaki and Miklossy and others have demonstrated a relationship between infection and amyloid as well. These comments are not to detract from the current report, but they are needed to provide an appropriate context in which to evaluate the current findings.


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    . Detection of bacterial antigens and Alzheimer's disease-like pathology in the central nervous system of BALB/c mice following intranasal infection with a laboratory isolate of Chlamydia pneumoniae. Front Aging Neurosci. 2014;6:304. Epub 2014 Dec 5 PubMed.

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  1. Like a Tiny Spider-Man, Aβ May Fight Infection by Cocooning Microbes