Abstract
The neurofibrillary tau pathology and amyloid deposits seen in Alzheimer’s disease (AD) also have been seen in bacteria-infected brains. However, few studies have examined the role of these bacteria in the generation of tau pathology. One suggested link between infection and AD is edentulism, the complete loss of teeth. Edentulism can result from chronic periodontal disease due to infection by Enterococcus faecalis. The current study assessed the ability to generate early Alzheimer-like neurofibrillary epitopes in primary rat cortical neurons through bacterial infection by E. faecalis. Seven-day old cultured neurons were infected with E. faecalis for 24 and 48 h. An upward molecular weight shift in tau by Western blotting (WB) and increased appearance of tau reactivity in cell bodies and degenerating neurites was found in the 48 h infection group for the antibody CP13 (phospho-Serine 202). A substantial increase in reactivity of Alz-50 was seen at 24 and 48 h after infection. Furthermore, extensive microtubule-associated protein 2 (MAP2) reactivity also was seen at 24 and 48 h post-infection. Our preliminary findings suggest a potential link between E. faecalis infection and intracellular changes that may help facilitate early AD-like neurofibrillary pathology. HighlightsEnterococcus faecalis used in the generation of AD neurofibrillary epitopes in rat.Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression.Infection by Enterococcus may play a role in early Alzheimer neurofibrillary changes.
Highlights
Neurofibrillary tau pathology and beta amyloid deposition are the classic defining biological markers of Alzheimer’s disease (AD)
Various types of spirochetes, including six periodontal pathogen spirochetes and Borrelia burgdorferi (MacDonald, 1986; MacDonald and Miranda, 1987; Miklossy, 1993; Riviere et al, 2002; Miklossy et al, 2004) and an obligate intracellular bacterium Chlamydophila (Chlamydia) pneumoniae (Balin et al, 1998, 2008; Hammond et al, 2010) have been detected and isolated from Alzheimer brain tissue, yet few studies have examined the involvement of these pathogens in the production of AD-like tau/neurofibrillary pathology (Miklossy et al, 2006)
It has been suggested that E. faecalis can travel from sites of dental infection to the brain (Mylona et al, 2012); making it an attractive candidate associated with AD pathology
Summary
Neurofibrillary tau pathology and beta amyloid deposition are the classic defining biological markers of Alzheimer’s disease (AD). Infection from Enterococcus faecalis, the bacteria most commonly associated with failed endodontic procedures (Sundqvist et al, 1998; Rocas et al, 2004; Zoletti et al, 2006; Al-Ahmad et al, 2010), secondary endodontic infections (Schirrmeister et al, 2009), urinary tract infections (Zoletti et al, 2006) and nosocomial infection (Courvalin, 2006), has been implicated in the pathogenesis of chronic periodontitis (Sun et al, 2012). These bacteria can form biofilms, making them extremely difficult to remove and allowing for cell microcolony formation which results in chronic infection (Mohamed and Huang, 2007; Arciola et al, 2008). It has been suggested that E. faecalis can travel from sites of dental infection to the brain (Mylona et al, 2012); making it an attractive candidate associated with AD pathology
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