Thursday, April 11, 2019

Porphyromonas Gingivalis Infections Underline Association of Periodontitis with Systemic Diseases

 



Since January of 2019 there has been a lot of talk about Alzheimer’s and the probable link between the disease and the bacteria Porphyromonas Gingivalis.  It seems that there are more and more pieces of the puzzle falling into place that show a definitive link.  Now there is a new study the is tying things even more closely together.
The study with is a work between the University of Louisville School of Dentistry and Poland’s University in Krakow, show what the researchers are calling “the strongest evidence of the link yet”.  The researchers performed examinations of brain tissue on deceased individuals some of whom suffered from Alzheimer’s and some who did not.
What they found was that Porphyromonas Gingivalis was much more common in the Alzheimer’s group than in the healthy group.  PG leaves a genetic marker call “gingipains” which is a positive indication of that the bacteria had been present.  
Here is the abstract:
Porphyromonas gingivalis, the keystone pathogen in chronic periodontitis, was identified in the brain of Alzheimer’s disease patients. Toxic proteases from the bacterium called gingipains were also identified in the brain of Alzheimer’s patients, and levels correlated with tau and ubiquitin pathology. Oral P. gingivalis infection in mice resulted in brain colonization and increased production of Aβ1–42, a component of amyloid plaques. Further, gingipains were neurotoxic in vivo and in vitro, exerting detrimental effects on tau, a protein needed for normal neuronal function. To block this neurotoxicity, we designed and synthesized small-molecule inhibitors targeting gingipains. Gingipain inhibition reduced the bacterial load of an established P. gingivalis brain infection, blocked Aβ1–42 production, reduced neuroinflammation, and rescued neurons in the hippocampus. These data suggest that gingipain inhibitors could be valuable for treating P. gingivalis brain colonization and neurodegeneration in Alzheimer’s disease.

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