Olsen Ingar, Singhrao Sim K
Institute of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.
Brain and Behavior Centre, Faculty of Clinical and Biomedical Sciences, School of Dentistry, University of Central Lancashire, Preston, UK.
J Oral Microbiol. 2020 Sep 16;12(1):1820834. doi: 10.1080/20002297.2020.1820834.
In late-onset Alzheimer disease (AD) pathogenesis, genes, infections and immunity could be significant factors. We have reviewed if the keystone periodontal pathogen may affect genes and microglia (primary immune cells in the brain) to promote AD development. Genes for apolipoprotein, clusterin, CD33, triggering receptor expressed on myeloid cells-2 (TREM-2), tyrosine kinase binding protein (TYR-OBP), and complement receptors can affect microglia. Most of these genes can also be affected by via its mastering of immune suppression. Besides, can affect microglia directly in several ways. Taken together, genetic predisposition, infection and microglia could promote neurodegeneration typical of that reported for AD.
在晚发性阿尔茨海默病（AD）的发病机制中，基因、感染和免疫可能是重要因素。我们回顾了关键的牙周病原体是否可能影响基因和小胶质细胞（大脑中的主要免疫细胞）以促进AD的发展。载脂蛋白、簇集蛋白、CD33、髓样细胞表达的触发受体2（TREM-2）、酪氨酸激酶结合蛋白（TYR-OBP）和补体受体的基因可影响小胶质细胞。这些基因中的大多数也可通过其对免疫抑制的掌控而受到影响。此外， 可通过多种方式直接影响小胶质细胞。综上所述，遗传易感性、 感染和小胶质细胞可促进AD所报道的典型神经退行性变。
原文中存在部分未明确表述的内容，用“ ”代替，翻译可能会存在一定局限性。
