[1] Sedghi LM, Bacino M, Kapila YL. Periodontal Disease: The Good, The Bad, and The Unknown[J]. Front Cell Infect Microbiol, 2021, 11: 766944. [2] Scheltens P, De Strooper B, Kivipelto M, et al. Alzheimer's disease[J]. Lancet, 2021, 397(10284): 1577-1590.[3] Harding A, Gonder U, Robinson SJ, et al. Exploring the Association between Alzheimer's Disease, Oral Health, Microbial Endocrinology and Nutrition[J]. Front Aging Neurosci, 2017, 9: 398.[4] Laugisch O, Johnen A, Maldonado A, et al. Periodontal pathogens and associated intrathecal antibodies in early stages of Alzheimer's disease[J]. J Alzheimers Dis, 2018, 66(1): 105-114.[5] Noble JM, Scarmeas N, Celenti RS, et al. Serum IgG antibody levels to periodontal microbiota are associated with incident Alzheimer disease[J]. PLoS One, 2014;9(12):e114959[6] Wang M, Cao J, Gong C, et al. Exploring the microbiota-Alzheimer's disease linkage using short-term antibiotic treatment followed by fecal microbiota transplantation[J]. Brain Behav Immun, 2021, 96: 227-238.[7] Kumar PS. From focal sepsis to periodontal medicine: a century of exploring the role of the oral microbiome in systemic disease[J]. J Physiol, 2017, 595(2): 465-476.[8] Gu L, Guo Z. Alzheimer's Aβ42 and Aβ40 form mixed oligomers with direct molecular interactions[J]. Biochem Biophys Res Commun, 2021, 534: 292-296.[9] Zhu H, Zhang W, Zhao Y, et al. GSK3beta-mediated tau hyperphosphorylation triggers diabetic retinal neurodegeneration by disrupting synaptic and mitochondrial functions[J]. Mol Neurodegener, 2018, 13(1): 62.[10] Tiwari S, Atluri V, Kaushik A, et al. Alzheimer's disease: pathogenesis, diagnostics, and therapeutics[J]. Int J Nanomedicine, 2019, 14: 5541- 5554.[11] Qin Q, Teng Z, Liu C, et al. TREM2, microglia, and Alzheimer's disease[J]. Mech Ageing Dev, 2021, 195(2): 111438.[12] Perea JR, Bolós M, Avila J. Microglia in Alzheimer's Disease in the Context of Tau Pathology[J]. Biomolecules, 2020, 10(10): 1439.[13] Itzhaki RF, Golde TE, Heneka MT, et al. Do infections have a role in the pathogenesis of Alzheimer disease[J]? Nat Rev Neurol, 2020, 16(4): 193-197.[14] Sochocka M, Zwolińska K, Leszek J. The Infectious Etiology of Alzheimer's Disease[J]. Curr Neuropharmacol, 2017, 15(7): 996-1009.[15] Merlini M, Kirabali T, Kulic L, et al. Extravascular CD3+ T cells in brains of Alzheimer disease patients correlate with Tau but not with amyloid pathology: an immunohistochemical study[J]. Neurodegener Dis, 2018, 18(1): 49-56.[16] St- Amour I, Bosoi CR, Pare I, et al. Peripheral adaptive immunity of the triple transgenic mouse model of Alzheimer's disease[J]. J Neuroinflammation, 2019, 16(1): 3. [17] Liu XX, Jiao B, Liao XX, et al. Analysis of Salivary Microbiome in Patients with Alzheimer's Disease[J]. J Alzheimers Dis, 2019, 72(2):633-640.[18] Kamer AR, Pushalkar S, Gulivindala D, et al. Periodontal dysbiosis associates with reduced CSF Aβ42 in cognitively normal elderly[J]. Alzheimers Dement (Amst), 2021, 13(1): e12172.[19] Wu YF, Lee WF, Salamanca E, et al. Oral Microbiota Changes in Elderly Patients, an Indicator of Alzheimer's Disease[J]. Int J Environ Res Public Health, 2021, 18(8): 4211.[20] Beydoun MA, Beydoun HA, Hossain S, et al. Clinical and Bacterial Markers of Periodontitis and Their Association with Incident All-Cause and Alzheimer's Disease Dementia in a Large National Survey[J]. J Alzheimers Dis, 2020, 75(1): 157-172.[21] Riviere GR, Riviere KH, Smith KS. Molecular and immunological evidence of oral Treponema in the human brain and their association with Alzheimer's disease[J]. Oral Microbiol Immunol, 2002, 17(2):113-8.[22] Poole S, Singhrao SK, Kesavalu L, et al. Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer's disease brain tissue[J]. J Alzheimers Dis, 2013, 36(4): 665-77.[23] Dominy SS, Lynch C, Ermini F, et al. Porphyromonas gingivalis in Alzheimer's disease brains: Evidence for disease causation and treatment with small-molecule inhibitors[J]. Sci Adv, 2019, 5(1): eaau3333.[24] Sweeney MD, Zhao Z, Montagne A, et al. Blood-Brain Barrier: From Physiology to Disease and Back[J]. Physiol Rev, 2019, 99(1): 21-78. [25] Kouki MA, Pritchard AB, Alder JE, et al. Do Periodontal Pathogens or Associated Virulence Factors Have a Deleterious Effect on the Blood-Brain Barrier, Contributing to Alzheimer's Disease[J]? J Alzheimers Dis, 2022, 85(3): 957-973.[26] Furutama D, Matsuda S, Yamawaki Y, et al. IL-6 Induced by Periodontal Inflammation Causes Neuroinflammation and Disrupts the Blood-Brain Barrier[J]. Brain Sci, 2020, 10(10): 679.[27] Brailoiu, Eugen, Shipsky, et al. Mechanisms of modulation of brain microvascular endothelial cells function by thrombin[J]. Brain Res, 2017, 1657:167-175.[28] Haditsch U, Roth T, Rodriguez L, et al. Alzheimer's Disease-Like Neurodegeneration in Porphyromonas gingivalis Infected Neurons with Persistent Expression of Active Gingipains[J]. J Alzheimers Dis, 2020, 75(4): 1361-1376.[29] Hu Y, Li H, Zhang J, Zhang X, Xia X, Qiu C, Liao Y, Chen H, Song Z, Zhou W. Periodontitis Induced by P. gingivalis-LPS Is Associated With Neuroinflammation and Learning and Memory Impairment in Sprague-Dawley Rats[J]. Front Neurosci, 2020, 14: 658.[30] Gu Y, Wu Z, Zeng F, et al. Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis Induces Bone Loss-Correlated Alzheimer's Disease-Like Pathologies in Middle-Aged Mice[J]. J Alzheimers Dis, 2020, 78(1): 61-74.[31] Qiu C, Yuan Z, He Z, et al. Lipopolysaccharide Preparation Derived From Porphyromonas gingivalis Induces a Weaker Immuno-Inflammatory Response in BV-2 Microglial Cells Than Escherichia coli by Differentially Activating TLR2/4-Mediated NF-κB/STAT3 Signaling Pathways[J]. Front Cell Infect Microbiol, 2021, 11: 606986.[32] Zekeridou A, Mombelli A, Cancela J, et al. Systemic inflammatory burden and local inflammation in periodontitis: What is the link between inflammatory biomarkers in serum and gingival crevicular fluid[J]? Clin Exp Dent Res, 2019, 5(2): 128-135.[33] Xie J, Gorlé N, Vandendriessche C, et al. Low-grade peripheral inflammation affects brain pathology in the AppNL-G-Fmouse model of Alzheimer's disease[J]. Acta Neuropathol Commun, 2021, 9(1): 163.[34] Evans ML, Gichana E, Zhou Y, et al. Bacterial Amyloids[J]. Methods Mol Biol. 2018, 1779: 267-288.[35] Van Gerven N, Van der Verren SE, Reiter DM, et al. The Role of Functional Amyloids in Bacterial Virulence[J]. J Mol Biol, 2018, 430(20): 3657-3684. [36] Laval K, Enquist LW. The Potential Role of Herpes Simplex Virus Type 1 and Neuroinflammation in the Pathogenesis of Alzheimer's Disease[J]. Front Neurol, 2021, 12: 658695.[37] Eimer WA, Vijaya Kumar DK, Navalpur Shanmugam NK, et al. Alzheimer's Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection[J]. Neuron, 2018, 99(1): 56-63.e3.[38] De Chiara G, Piacentini R, Fabiani M, et al. Recurrent herpes simplex virus-1 infection induces hallmarks of neurodegeneration and cognitive deficits in mice[J]. PLoS Pathog, 2019, 15(3): e1007617.[39] Zhang J, Zheng Y, Luo Y, et al. Curcumin inhibits LPS-induced neuroinflammation by promoting microglial M2 polarization via TREM2/ TLR4/ NF-κB pathways in BV2 cells[J]. Mol Immunol, 2019, 116: 29-37.[40] Sun ZZ, Li XY, Wang S, et al. Bidirectional interactions between curcumin and gut microbiota in transgenic mice with Alzheimer's disease[J]. Appl Microbiol Biotechnol, 2020, 104(8): 3507-3515.[41] Harding A, Ribinson S, Singhrao SK. Can better management of periodontal disease delay the onset and Progression of Alzheimer's disease?[J]. J Alzheimers Dis, 2017, 58(2): 337-348.[42] Schwahn C, Frenzel S, Holtfreter B, et al. Alzheimer's Disease Neuroimaging Initiative. Effect of periodontal treatment on preclinical Alzheimer's disease-Results of a trial emulation approach[J]. Alzheimers Dement, 2022, 18(1): 127-141. |