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Purpose of Review

Chronic diseases remain a daunting challenge for clinicians and researchers alike. While difficult to completely understand, most chronic diseases, including late-onset dementias, are thought to arise as an interplay between host genetic factors and environmental insults. One of the most diverse and ubiquitous environmental insults centers on infectious agents. Associations of infectious agents with late-onset dementia have taken on heightened importance, including our investigations of infection by the intracellular respiratory bacterium, Chlamydia pneumoniae (Cpn), in late-onset dementia of the Alzheimer’s type.

Recent Findings

Over the last two decades, the relationship of this infection to pathogenesis in late-onset dementia has become much clearer. This clarity has resulted from applying contemporary molecular genetic, biochemical, immunochemical, and cell culture techniques to analysis of human brains, animal models, and relevant in vitro cell culture systems. Data from these studies, taken in aggregate form, now can be applied to evaluation of proof of concept for causation of this infection with late-onset disease. In this evaluation, modifications to the original Koch postulates can be useful for elucidating causation.


All such relevant studies are outlined and summarized in this review, and they demonstrate the utility of applying modified Koch postulates to the etiology of late-onset dementia of the Alzheimer’s type. Regardless, it is clear that even with strong observational evidence, in combination with application of modifications of Koch’s postulates, we will not be able to conclusively state that Cpn infection is causative for disease pathogenesis in late-onset dementia. Moreover, this conclusion obtains as well for the putative causation of this condition by other pathogens, including herpes simplex virus type 1, Borrelia burgdorferi, and Porphyromonas gingivalis.

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This article was published in Bacteriology.

The published version is available at

Copyright 2020 The Author(s). CC BY 4.0.