Chronic Porphyromonas gingivalis infection accelerates the occurrence of age-related granules in ApoE^–/– mice brains

References

• Akiyama H, Kameyama M, Akiguchi I, et al. Periodic acid-Schiff (PAS)-positive, granular structures increase in the brain of senescence accelerated mouse (SAM). Acta Neuropathol. 1986;72:1–10.
   Web of Science ®Google Scholar
• Jucker M, Walker LC, Schwarb P, et al. Age-related deposition of glia-associated fibrillar material in brains of C57BL/6 mice. Neuroscience. 1994;60:875–889.
   PubMed Web of Science ®Google Scholar
• Kuo H, Ingram DK, Walker LC, et al. Similarities in the age-related hippocampal deposition of periodic acid-schiff-positive granules in the senescence-accelerated mouse P8 and C57BL/6 mouse strains. Neuroscience. 1996;74:733–740.
   Web of Science ®Google Scholar
• Miyamoto M, Kiyota Y, Yamazaki N, et al. Age-related changes in learning and memory in the senescence-accelerated mouse (SAM). Physiol Behav. 1986;38:399–406.
   PubMed Web of Science ®Google Scholar
• Ma Q, Qiang J, Gu P, et al. Age-related autophagy alterations in the brain of senescence accelerated mouse prone 8 (SAMP8) mice. Exp Gerontol. 2011;46:533–541. DOI:10.1016/j.exger.2011.02.006
   PubMed Web of Science ®Google Scholar
• Su JH, Cummings BJ, Cotman CW. Localization of heparan sulfate glycosaminoglycan and proteoglycan core protein in aged brain and Alzheimer’s disease. Neuroscience. 1992;51:801–813.
   PubMed Web of Science ®Google Scholar
• Jucker M, Walker LC, Kuo H, et al. Age related fibrillary deposits in brains of C57BL/6 mice. A review of localisation, staining characteristics, and strain specificity. Mol Neurobiol. 1994;125–133. DOI:10.1007/BF02816112
   Web of Science ®Google Scholar
• Snow AD, Wright TN, Nochlin D, et al. Immunocolocalization of heparin sulfate proteoglycans to the prion protein amyloid plaques of Gerstmann-Straussler syndrome, Creutzfeldt-Jakob disease and scrapie. Lab Invest. 1990;63:601–611.
   PubMed Web of Science ®Google Scholar
• Snow AD, Sekiguchi RT, Nochlin D, et al. Heparan sulfate proteoglycan in diffuse plaques of hippocampus but not of cerebellum in Alzheimer’s disease brain. Am J Pathol. 1994;144:337–347.
   PubMed Web of Science ®Google Scholar
• Montagne A, Barnes SR, Sweeney MD, et al. Blood-brain barrier breakdown in the aging human hippocampus. Neuron. 2015;85:296–302. DOI:10.1016/j.neuron.2014.12.032
   PubMed Web of Science ®Google Scholar
• Hafezi-Moghadam A, Thomas KL, Wagner DD. ApoE deficiency leads to a progressive age-dependent blood-brain barrier leakage. Am J Physiol Cell Physiol. 2007;292:C1256–C1262. DOI:10.1152/ajpcell.00563.2005
   Web of Science ®Google Scholar
• Sohet F, Daneman R. Genetic mouse models to study blood-brain barrier development and function. Fluids Barriers CNS. 2013;10:3. PMID:23305182. DOI:10.1186/2045-8118-10-3
   Google Scholar
• Methia N, Andre P, Hafezi-Moghadam A, et al. ApoE deficiency compromises the blood brain barrier especially after injury. Mol Med. 2001;7:810–815.
   PubMed Web of Science ®Google Scholar
• Laskowitz DT, Lee DM, Schmechel D, et al. Altered immune responses in apolipoprotein E-deficient mice. J Lipid Res. 2000;41:613–620.
   PubMed Web of Science ®Google Scholar
• Vitek MP, Brown CM, Colton CA. APOE genotype-specific differences in the innate immune response. Neurobiol Aging. 2009;30:1350–1360. DOI:10.1016/j.neurobiolaging.2007.11.014
   PubMed Web of Science ®Google Scholar
• Poole S, Singhrao SK, Chukkapalli S, et al. Active invasion of an oral bacterium and infection-induced complement activation in ApoEnull mice brains. J Alzheimers Dis. 2015;43:67–80.
   PubMed Web of Science ®Google Scholar
• 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 Alzheimers Dis. 2013;36:665–677. DOI:10.3233/JAD-121918
   PubMed Web of Science ®Google Scholar
• Velsko IM, Chukkapalli SS, Rivera MF, et al. Active invasion of oral and aortic tissues by Porphyromonas gingivalis in mice causally links periodontitis and atherosclerosis. PLOS One. 2014;9:e97811. DOI:10.1371/journal.pone.0097811
   PubMed Web of Science ®Google Scholar
• Veurink G, Liu D, Taddei K, et al. Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidants. Free Radic Biol Med. 2003;34:1070–1077.
   PubMed Web of Science ®Google Scholar
• Sunde PT, Olsen I, Gobel UB, et al. Fluoresence in situ hybridization (FISH) for direct visualization of bacteria in periapical lesions of asymptomatic root-filled teeth. Microbiology. 2003;149:1095–1102. DOI:10.1099/mic.0.26077-0
   PubMed Web of Science ®Google Scholar
• Singhrao S, Cole G, Henderson WJ, et al. White embedding allows a multi-method approach to the analysis of brain tissue from patients with Alzheimer’s disease. J Histochem. 1990;22:257–268. DOI:10.1007/BF01387181
   Web of Science ®Google Scholar
• Miklossy J, Darekar P, Gern L, et al. Bacterial peptidoglycan in neuritic plaques in Alzheimer’s disease. Azheimer’s Res. 1996;2:95–100.
   Google Scholar
• Fullerton SM, Shirman GA, Strittmatter WJ, et al. Impairment of the blood-nerve and blood-brain barriers in apolipoprotein E knockout mice. Exp Neurol. 2001;169:13–22. DOI:10.1006/exnr.2001.7631
   PubMed Web of Science ®Google Scholar
• Singhrao SK, Neal JW, Rushmere NK, et al. Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis. Am J Pathol. 2000;157:905–918. DOI:10.1016/S0002-9440(10)64604-4
   PubMed Web of Science ®Google Scholar
• Roselaar SE, Daugherty A. Apolipoprotein E-deficient mice have impaired innate immune responses to Listeria monocytogenes in vivo. J Lipid Res. 1998;39:1740–1743.
   Web of Science ®Google Scholar
• de Bont N, Netea MG, Demacker PN, et al. Apolipoprotein E knock-out mice are highly susceptible to endotoxemia and Klebsiella pneumoniae infection. J Lipid Res. 1999;40:680–685.
   PubMed Web of Science ®Google Scholar
• Jucker M, Walker LC, Martin LJ, et al. Age-associated inclusions in normal and transgenic mouse brain. Science. 1992;255:1443–1445.
   PubMed Web of Science ®Google Scholar
• Cana A, Herder V, Hansmann F, et al. Spitzbarth. Characterization of periodic-acid-Schiff-positive granular deposits in the hippocampus of SJL/J mice. Toxicol Pathol. 2015;43:737–742. DOI:10.1177/0192623314564254
   Web of Science ®Google Scholar
• MacDonald AB, Miranda JM. Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987;18:759–761.
   Web of Science ®Google Scholar
• Miklossy J. Chronic inflammation and amyloidogenesis in Alzheimer’s disease - role of spirochetes. J Alzheimer Dis. 2008;13:381–391.
   Web of Science ®Google Scholar
• Balin B, Little C, Hammond C, et al. Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease. J Alzheimers Dis. 2008;13:371–380.
   PubMed Web of Science ®Google Scholar
• Riviere GR, Riviere K, Smith K. Molecular and immunological evidence of oral Treponema in the human brain and their association with Alzheimer’s disease. Oral Microbiol Immunol. 2002;17:113–118.
   PubMedGoogle Scholar
• Dunn N, Mullee M, Perry V, et al. Association between dementia and infectious disease: evidence from a case-control study. Alzheimer Dis Assoc Disord. 2005;19:91–94.
   Web of Science ®Google Scholar
• Holmes C, El-Okl M, Williams AL, et al. Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer’s disease. J Neurol Neurosurg Psychiatry. 2003;74:788–789. DOI:10.1136/jnnp.74.6.788
   PubMed Web of Science ®Google Scholar
• Olsen I, Yilmaz Ö. Modulation of inflammasome activity by Porphyromonas gingivalis in periodontitis and associated systemic diseases. J Oral Microbiol. 2016;8:30385. DOI:10.3402/jom.v8.30385
   PubMed Web of Science ®Google Scholar
• Olsen I, Singhrao SK. Inflammasome involvement in Alzheimer’s disease. J Alzheimers Dis. 2016;54:45–53. DOI:10.3233/JAD-160197
   Web of Science ®Google Scholar
• Ophir G, Amariglio N, Jacob-Hirsch J, et al. Apolipoprotein E4 enhances brain inflammation by modulation of the NF-κB signaling cascade. Neurobiol Dis. 2005;20:709–718. DOI:10.1016/j.nbd.2005.05.002
   PubMed Web of Science ®Google Scholar
• Tsoi LM, Wong KY, Liu YM. Ho YY Apoprotein E isoform-dependent expression and secretion of pro-inflammatory cytokines TNF-α and IL-6 in macrophages. Arch Biochem Biophys. 2007;460:33–40. DOI:10.1016/j.abb.2007.01.019
   Web of Science ®Google Scholar
• Singhrao SK, Neal JW, Newman GR. Corpora amylacea could be an indicator of neurodegeneration. Neuropathol Appl Neurobiol. 1993;19:269–276.
   PubMed Web of Science ®Google Scholar
• Ramsey HJ. Ultrastructure of corpora amylacea. J Neuropathol Exp Neurol. 1965;24:29–39. DOI:10.1097/00005072-196501000-00003
   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. 2015. DOI:10.1038/jcbfm.2015.44
   Web of Science ®Google Scholar
• Miklossy J. Historic evidence to support a causal relationship between spirochetal infections and Alzheimer’s disease. Front Aging Neurosci. 2015;7:46. DOI:10.3389/fnagi.2015.00046
   PubMed Web of Science ®Google Scholar
• Kumar DK, Choi SH, Washicosky KJ, et al. Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease. Sci Transl Med. 2016;8: 340ra72. DOI:10.1126/scitranslmed.aaf1059
   Web of Science ®Google Scholar
• Miklossy J. Bacterial amyloid and DNA are important constituents of senile plaques: further evidence of the spirochetal and biofilm nature of senile plaques. J Alzheimer’s Dis. 2016;53:1459–1473. DOI:10.3233/JAD-160451
   PubMed Web of Science ®Google Scholar