JAD: Chinese and Japanese scientists reveal that periodontitis may cause Alzheimer's disease

December 5, 2019 / BIOON / - -- Alzheimer's disease is a public health crisis The cause of the disease is still unknown and there is no effective way to treat it Nearly six million people in the United States suffer from Alzheimer's disease, and as the population ages, the number is expected to reach 14 million by 2060 According to the Alzheimer's Association, the health care system spends more than $25 trillion a year on Alzheimer's patients The disease also places a heavy burden on family members Alzheimer's disease is one of the most common forms of dementia and neurodegeneration Alzheimer's disease is characterized by the deposition of toxic protein aggregates in the brain called β - amyloid (a β) plaques and tau tangles, as well as cognitive decline and dementia In 2019, Atsushi Aoyagi et al Proposed that two proteins, a β and tau, which are crucial to the pathology of Alzheimer's disease, play a role as prions - proteins with abnormal structure by forcing normal proteins to show the same fold shape and spread in tissues like infectious diseases (Science Translational Medicine, 2019, doi:10.1126/scitranslmed.aat8462）。 In other words, Alzheimer's disease is actually a double prion disease It has been found that chronic systemic exposure to lipopolysaccharide of Porphyromonas gingivalis can induce a β accumulation in the brain of middle-aged mice On the other hand, recent studies have shown that a β in blood circulation can be transferred to the brain However, it is not clear whether chronic systemic Porphyromonas gingivalis infection is related to a β metabolism in peripheral tissues In a new study, researchers from institutions such as Jilin University of China and Kyushu University of Japan speculated that chronic Porphyromonas gingivalis infection expanded the a β pool in peripheral inflammatory tissues, thus promoting the accumulation of a β in the brain of patients with periodontitis They found that the increased expression of IL-1 β, a β pp770, CatB, a β 1-42 and a β 3-42 mainly occurred in liver macrophages of mice infected with Porphyromonas gingivalis The related research results were recently published in Journal of Alzheimer's disease The title of the paper is "Porphyromonas ginalivalis infection inductions amino - β accumulation in monocytes / macrophases" The corresponding authors of this paper are professor Yanmin Zhou, School of Stomatology, Jilin University, Professor Zhou Wu and Professor junjunjuni Ni, School of Dentistry, Kyushu University Brain of patients with Alzheimer's disease, image from Wikimedia Commons They found that blocking cathepsin B and NF - κ B significantly inhibited the expression of IL-1 β, a β pp770, a β 1-42 and a β 3-42 induced by Porphyromonas gingivalis in RAW264.7 cells A β 3-42, rather than a β 1-42, induces a large number of macrophages to die, and the phagocytic decline induced by a β 3-42 is often higher than that induced by a β 1-42 In addition, they detected the expression of a β pp770, CatB, a β 1-42 and a β 3-42 in macrophages from gingival tissue of patients with periodontitis, and found a β in macrophages from gingival tissue of patients with periodontitis for the first time These findings indicate that chronic systemic Porphyromonas gingivalis infection induces a β accumulation in inflammatory monocytes / macrophages by activating CatB / NF - κ B signaling pathway, which indicates that monocytes / macrophages can be used as a β circulating pool in patients with periodontitis In conclusion, CatB may be a new therapeutic target to prevent the onset and pathological progress of periodontitis related Alzheimer's disease (BIOON Com) reference: ran Nie et al Porphyromonas gingivalis infection causes amino - β accumulation in monocytes / macrophases Journal of Alzheimer's disease, 2019, DOI: 10.3233/jad-190298