There is good mechanistic evidence for the bacteria responsible for gum disease, periodontitis, to contribute directly to age-related inflammation in the heart, brain, and other organs, and thus raise the risk of suffering cardiovascular disease, Alzheimer’s disease, and numerous other conditions that are accelerated by chronic inflammation. In the case of Alzheimer’s disease, is the effect size due to periodontitis large enough to care about in comparison to other contributing causes, however? Some research suggests that the increase in risk of Alzheimer’s is modest, but this is still a point that can be argued either way.

Alzheimer’s disease (AD) is the most common cause of dementia, and it exhibits pathological properties such as deposition of extracellular amyloid β (Aβ) and abnormally phosphorylated tau in nerve cells and a decrease of synapses. Conventionally, drugs targeting Aβ and its related molecules have been developed on the basis of the amyloid cascade hypothesis, but sufficient effects on the disease have not been obtained in past clinical trials. On the other hand, it has been pointed out that chronic inflammation and microbial infection in the brain may be involved in the pathogenesis of AD.

Recently, attention has been focused on the relationship between the periodontopathic bacterium Porphylomonas gingivalis and AD. P. gingivalis and its toxins have been detected in autopsy brain tissues from patients with AD. In addition, pathological conditions of AD are formed or exacerbated in mice infected with P. gingivalis. Compounds that target the toxins of P. gingivalis ameliorate the pathogenesis of AD triggered by P. gingivalis infection. These findings indicate that the pathological condition of AD may be regulated by controlling the bacteria in the oral cavity and the body. In the current aging society, the importance of oral and periodontal care for preventing the onset of AD will increase.