Gum Disease Bacteria Implicated in Alzheimer’s Diseaseby Neuroscience News |
Researchers have implicated Porphyromonas gingivalis, a bacteria commonly associated with gum disease, in Alzheimer's pathology. The study reports oral Pg infections leads to a colonization and increased production of amyloid beta.
Summary: Researchers have implicated Porphyromonas gingivalis, a bacteria commonly associated with gum disease, in Alzheimer’s pathology. The study reports oral Pg infections leads to a colonization and increased production of amyloid beta.
Source: University of Louisville.
New science uncovers how an unlikely culprit, Porphyromonas gingivalis (Pg) – the bacterium commonly associated with chronic gum disease – appears to drive Alzheimer’s disease (AD) pathology.
A paper published today in Science Advances details how researchers identified Pg in the brains of patients with AD.
University of Louisville researcher Jan Potempa, Ph.D., Department of Oral Immunology and Infectious Diseases in the School of Dentistry, was part of the team of international scientists led by Cortexyme Inc., a privately held, clinical-stage pharmaceutical company.
According to Potempa, although infectious agents have been implicated in the development and progression of Alzheimer’s disease, the evidence of causation hasn’t been convincing.
However, “we now have strong evidence connecting P. gingivalis and Alzheimer’s pathogenesis, but more research needs to be done.
“An even more notable aspect of this study is demonstration of the potential for a class of molecule therapies targeting major virulence factors to change the trajectory of AD, which seems to be epidemiologically and clinically associated with periodontitis,” Potempa said.
In animal models, oral Pg infection led to brain colonization and increased production of amyloid beta (Aβ), a component of the amyloid plaques commonly associated with AD.
The study team also found the organism’s toxic enzymes, or gingipains, in the neurons of patients with AD. Gingipains are secreted and transported to outer bacterial membrane surfaces and have been shown to mediate the toxicity of Pg in a variety of cells. The team correlated the gingipain levels with pathology related to two markers: tau, a protein needed for normal neuronal function, and ubiquitin, a small protein tag that marks damaged proteins.
Seeking to block Pg-driven neurotoxicity, Cortexyme set out to design a series of small molecule therapies targeting Pg gingipains. In preclinical experiments detailed in the paper, researchers demonstrated that by inhibiting the compound COR388, there was reduced bacterial load of an established Pg brain infection, blocked Aβ42 production, reduced neuroinflammation and protected neurons in the hippocampus – the part of the brain that mediates memory and frequently atrophies early in the development of AD.
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