Possible effects of Porphyromonas gingivalis on the blood–brain barrier in Alzheimer’s disease

References

• Yamazaki Y, Kanekiyo T. Blood-brain barrier dysfunction and the pathogenesis of Alzheimer’s disease. Int J Mol Sci. 2017;18(9):1965.
   PubMed Web of Science ®Google Scholar
• Zenaro E, Piacentino G, Constantin G. The blood-brain barrier in Alzheimer’s disease. Neurobiol Dis. 2017;107:41–56.
   PubMed Web of Science ®Google Scholar
• Erickson MA, Banks WA. Blood-brain barrier dysfunction as a cause and consequence of Alzheimer’s disease. J Cereb Blood Flow Metab. 2013;33(10):1500–1513.
   PubMed Web of Science ®Google Scholar
• Michalicova A, Majerova P, Kovac A. Tau protein and its role in blood-brain barrier dysfunction. Front Mol Neurosci. 2020;13:570045.
   PubMed Web of Science ®Google Scholar
• Cai Z, Qiao P-F, Wan C-Q, et al. Role of blood-brain barrier in Alzheimer’s disease. J Alzheimers Dis. 2018;63(4):1223–1234.
   PubMed Web of Science ®Google Scholar
• Socransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25:134–144.
   PubMed Web of Science ®Google Scholar
• Hajishengallis G, Darveau RP, Curtis MA. The keystone-pathogen hypothesis. Nat Rev Microbiol. 2012;10:717–725.
   PubMed Web of Science ®Google Scholar
• Darveau RP, Hajishengallis G, Curtis MA. Porphyromonas gingivalis as a potential community activist. J Dent Res. 2012;91:816–820.
   PubMed Web of Science ®Google Scholar
• Hajishengallis G, Chavakis T. Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities. Nat Rev Immunol. 2021;28:1–15.
   Google Scholar
• Tomás I, Diz P, Tobias A, et al. Periodontal health status and bacteraemia from daily oral activities: systematic review/meta-analysis. J Clin Periodontol. 2012;39:213–228.
   PubMed Web of Science ®Google Scholar
• Dhotre S, Jahagirdar V, Suryawanshi N, et al. Assessment of periodontitis and its role in viridans streptococcal bacteremia and infective endocarditis. Indian Heart J. 2018;70:225–232.
   PubMedGoogle Scholar
• Olsen I, Singhrao SK. Can oral infection be a risk factor for Alzheimer’s disease? J Oral Microbiol. 2015;7:29143.
   PubMed Web of Science ®Google Scholar
• Panza F, Lozupone M, Solfrizzi V, et al. Time to test antibacterial therapy in Alzheimer’s disease. Brain. 2019;142:2905–2929.
   PubMed Web of Science ®Google Scholar
• 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. Sci Adv. 2019;5:eaau3333.
   PubMed Web of Science ®Google Scholar
• Varatharaj A, Galea I. The blood-brain barrier in systemic inflammation. Brain Behav Immun. 2017;60:1–12.
   PubMed Web of Science ®Google Scholar
• Deane R, Sagare A, Zlokovic BV. The role of the cell surface LRP and soluble LRP in blood-brain barrier Abeta clearance in Alzheimer’s disease. Curr Pharm Des. 2008;14(16):1601–1605.
   PubMed Web of Science ®Google Scholar
• Sagare AP, Deane R, Zlokovic BV. Low-density lipoprotein receptor-related protein 1: a physiological Aβ homeostatic mechanism with multiple therapeutic opportunities. Pharmacol Ther. 2012;136(1):94–105.
   PubMed Web of Science ®Google Scholar
• Jaeger LB, Dohgu S, Hwang MC, et al. Testing the neurovascular hypothesis of Alzheimer’s disease: LRP-1 antisense reduces blood-brain barrier clearance, increases brain levels of amyloid-beta protein, and impairs cognition. J Alzheimers Dis. 2009;17(3):553–570.
   PubMed Web of Science ®Google Scholar
• Rauch JN, Luna G, Guzman E, et al. LRP1 is a master regulator of tau uptake and spread. Nature. 2020;580:381–385.
   PubMed Web of Science ®Google Scholar
• Wan W, Chen H, Li Y. The potential mechanisms of Aβ-receptor for advanced glycation end-products interaction disrupting tight junctions of the blood-brain barrier in Alzheimer’s disease. Int J Neurosci. 2014;124(2):75–81.
   PubMed Web of Science ®Google Scholar
• Zeng F, Liu Y, Huang W, et al. Receptor for advanced glycation end products up‐regulation in cerebral endothelial cells mediates cerebrovascular‐related amyloid β accumulation after Porphyromonas gingivalis infection. J Neurochem. 2020. DOI:https://doi.org/10.1111/jnc.15096
   Google Scholar
• Evin G, Zhu A, Holsinger RMD, et al. Proteolytic processing of the Alzheimer’s disease amyloid precursor protein in brain and platelets. J Neurosci Res. 2003;74(3):386–392.
   PubMed Web of Science ®Google Scholar
• Nie R, Wu Z, Ni J, et al. Porphyromonas gingivalis infection induces amyloid-beta accumulation in monocytes/macrophages. J Alzheimer’s Dis. 2019;72:479–494.
   PubMed Web of Science ®Google Scholar
• Olsen I, Singhrao SK. Porphyromonas gingivalis infection may contribute to systemic and intracerebral amyloid-beta: implications for Alzheimer’s disease onset. Expert Rev Anti-Infect Ther. 2020;18(11):1063–1066.
   PubMed Web of Science ®Google Scholar
• Liu J, Wang Y, Guo J, et al. Salvianolic acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ levels in Porphyromonas gingivalis-infected mice. Aging (Albany NY). 2020;12(11):101117–110128.
   Google Scholar
• Tang Z, Liang D, Cheng M, et al. Effects of Porphyromonas gingivalis and its underlying mechanisms on Alzheimer-like tau hyperphosphorylation in Sprague-Dawley rats. J Mol Neurosci. 2021;71(1):89–100.
   PubMedGoogle Scholar
• Muldoon LL, Alvarez JI, Begley DJ, et al. Immunologic privilege in the central nervous system and the blood-brain barrier. J Cereb Blood Flow Metab. 2013;33(1):13–21.
   PubMed Web of Science ®Google Scholar
• Liu Y, Wu Z, Zhang X, et al. Leptomeningeal cells transduce peripheral macrophages inflammatory signal to microglia in reponse to Porphyromonas gingivalis LPS. Mediators Inflamm. 2013;2013:407562.
   PubMed Web of Science ®Google Scholar
• Wu Z, Nakanishi H. Lessons from microglia aging for the link between inflammatory bone disorders and Alzheimer’s disease. J Immunol Res. 2015;2015:471342.
   PubMed Web of Science ®Google Scholar
• Wang Y, Gao Y, Li X, et al. Coniferyl aldehyde inhibits the inflammatory effects of leptomeningeal cells by suppressing the JAK2 signaling. BioMed Res Int. 2020:4616308.
   PubMed Web of Science ®Google Scholar
• Chiba T, Yamada M, Aiso S. Targeting the JAK2/STAT3 axis in Alzheimer’s disease. Expert Opin Ther Target. 2009;13:1155–1167.
   PubMed Web of Science ®Google Scholar
• Mei F, Xie M, Huang X, et al. Porphyromonas gingivalis and its systemic impact: current status. Pathogens. 2020;9(11):944.
   PubMed Web of Science ®Google Scholar
• Olsen I, Taubman MA, Singhrao SK. Porphyromonas gingivalis suppresses adaptive immunity in periodontitis, atherosclerosis, and Alzheimer’s disease. J Oral Microbiol. 2016;8:33029.
   PubMed Web of Science ®Google Scholar
• Slaney JM, Gallagher A, Aduse-Opoku J, et al. Mechanisms of resistance of Porphyromonas gingivalis to killing by serum complement. Infect Immun. 2006;74:5352–5361.
   PubMed Web of Science ®Google Scholar
• Salloway S, Gur T, Berzin T, et al. Effect of APOE genotype on microvascular basement membrane in Alzheimer’s disease. J Neurol Sci. 2002;203-204:183–187.
   PubMed Web of Science ®Google Scholar
• Hultman K, Strickland S, Norris EH, et al. The APOE έ4/έ4 genotype potentiates vascular fibrin(ogen) deposition of amyloid-laden vessels in the brains of Alzheimer’s disease patients. J Cereb Blood Flow Metab. 2013;33(8):1251–1258.
   PubMed Web of Science ®Google Scholar
• Halliday MR, Rege SV, Ma Q, et al. Accelerated pericyte degeneration and blood–brain barrier breakdown in apolipoprotein E4 carriers with Alzheimer’s disease. J Cereb Blood Flow Metab. 2016;36(1):216–227.
   PubMed Web of Science ®Google Scholar
• Montagne A, Nation DA, Sagare AP, et al. APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline. Nature. 2020;581(7806):71–76.
   PubMed Web of Science ®Google Scholar
• Armulik A, Genové G, Mäe M, et al. Pericytes regulate the blood-brain barrier. Nature. 2010;468:557–561.
   PubMed Web of Science ®Google Scholar
• Nikolakopoulou AM, Montagne A, Kisler K, et al. Pericyte loss leads to circulatory failure and pleiotrophin depletion causing neuron loss. Nat Neurosci. 2019;22(7):1089–1098.
   PubMed Web of Science ®Google Scholar
• Riphagen JM, Ramakers IHGM, Freeze WM, et al. Linking APOE-ε4, blood-brain barrier dysfunction, and inflammation to Alzheimer’s pathology. Neurobiol Aging. 2020;85:96–103.
   PubMed Web of Science ®Google Scholar
• Alata W, Ye Y, St-Amour I, et al. Human apolipoprotein E ɛ4 expression impairs cerebral vascularization and blood-brain barrier function in mice. J Cereb Blood Flow Metab. 2015;35(1):86–94.
   PubMed Web of Science ®Google Scholar
• Carter C. Alzheimer’s disease: APP, gamma secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and their relationships with Herpes simplex, C. pneumoniae, other suspect pathogens, and the immune system. Int J Alzheimers Dis. 2011;2011:501862.
   PubMedGoogle Scholar
• Muñoz SS, Garner B, Ooi L. Understanding the role of ApoE fragments in Alzheimer’s disease. Neurochem Res. 2019;44:1297–1305.
   PubMed Web of Science ®Google Scholar
• Lönn J, Ljunggren S, Klarström-Engström K. Lipoprotein modifications by gingipains of Porphyromonas gingivalis. J Periodontal Res. 2018;53(3):403–413.
   PubMed Web of Science ®Google Scholar
• O’Connor DM, Boulis NM. Gene therapy for neurodegenerative diseases. Trends Mol Med. 2015;21(8):504–512.
   PubMed Web of Science ®Google Scholar
• Sudhakar V, Richardson RM. Gene therapy for neurodegenerative diseases. Neurotherapeutics. 2019;16(1):166–175.
   PubMed Web of Science ®Google Scholar