Research groups such as Kyushu University have discovered that "amyloid β (Aβ)," the main component of amyloid plaque in the brain found in Alzheimer-type dementia, is produced in the gums of human periodontal disease.
Previous clinical studies have shown that there is a positive correlation between the prevalence of periodontal disease and cognitive decline.In addition, the component of gingivalis (Pg), which is the causative bacterium of periodontal disease, has been detected in the brains of patients with Alzheimer-type dementia, and its involvement in periodontal disease in Alzheimer-type dementia has attracted attention.
This research group analyzed the periodontal tissue of human periodontal disease and discovered that Aβ is produced from macrophages, which are a type of cell responsible for inflammation and immune function.Furthermore, in the liver of mice to which Pg bacteria were systemically administered, Aβ was induced in inflamed macrophages.
Therefore, when the Aβ metabolism in the liver infected with Pg bacteria was analyzed, a significant increase in cathepsin B, which is an Aβ-producing enzyme, was observed.From this, the research group who thought that inflammatory macrophages caused by Pg bacteria induce Aβ production depending on cathepsin B can significantly suppress Aβ production by cathepsin B-specific inhibitors in the analysis using cultured macrophages. Succeeded in showing.
Until now, it has been thought that Aβ is produced and accumulated in the brain to form senile plaques. It suggests that it can be a resource for.
In the future, by targeting cathepsin B as a new therapeutic target, it is expected to realize "preemptive medicine" that delays the onset and progression of Alzheimer-type dementia due to periodontal disease.
Paper information:[Journal of Alzheimer's Disease] Porphyromonas gingivalis Infection Induces Amyloid-β Accumulation in Monocytes / Macrophages
