Journal of Inflammation Research (2020-06-01)

Periodontal Disease and Periodontal Disease-Related Bacteria Involved in the Pathogenesis of Alzheimer’s Disease

  • Matsushita K,
  • Yamada-Furukawa M,
  • Kurosawa M,
  • Shikama Y

Journal volume & issue
Vol. Volume 13
pp. 275 – 283

Abstract

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Kenji Matsushita, Masae Yamada-Furukawa, Mie Kurosawa, Yosuke Shikama Department of Oral Disease Research, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, JapanCorrespondence: Kenji MatsushitaDepartment of Oral Disease Research, National Center for Geriatrics and Gerontology, 7-430 Morioka-Chou, Obu, Aichi 474-8511, JapanEmail [email protected]: 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.Keywords: Porphylomonas gingivalis, cognitive decline, amyloid β, blood-brain barrier, vascular inflammation

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