Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with Enterococcus faecalis
Identifieur interne : 006351 ( Ncbi/Checkpoint ); précédent : 006350; suivant : 006352Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with Enterococcus faecalis
Auteurs : Robert Underly [États-Unis] ; Mee-Sook Song [États-Unis] ; Gary L. Dunbar [États-Unis] ; Charles L. Weaver [États-Unis]Source :
- Frontiers in Aging Neuroscience [ 1663-4365 ] ; 2016.
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 Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression. Infection by
Url:
DOI: 10.3389/fnagi.2015.00259
PubMed: 26834627
PubMed Central: 4720002
Affiliations:
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with <italic>Enterococcus faecalis</italic>
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<author><name sortKey="Underly, Robert" sort="Underly, Robert" uniqKey="Underly R" first="Robert" last="Underly">Robert Underly</name>
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<author><name sortKey="Song, Mee Sook" sort="Song, Mee Sook" uniqKey="Song M" first="Mee-Sook" last="Song">Mee-Sook Song</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Field Neurosciences Institute</institution>
<country>Saginaw, MI, USA</country>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Dunbar, Gary L" sort="Dunbar, Gary L" uniqKey="Dunbar G" first="Gary L." last="Dunbar">Gary L. Dunbar</name>
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<author><name sortKey="Weaver, Charles L" sort="Weaver, Charles L" uniqKey="Weaver C" first="Charles L." last="Weaver">Charles L. Weaver</name>
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<series><title level="j">Frontiers in Aging Neuroscience</title>
<idno type="eISSN">1663-4365</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p>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 <italic>Enterococcus faecalis</italic>
. The current study assessed the ability to generate early Alzheimer-like neurofibrillary epitopes in primary rat cortical neurons through bacterial infection by <italic>E. faecalis</italic>
. Seven-day old cultured neurons were infected with <italic>E. faecalis</italic>
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 <italic>E. faecalis</italic>
infection and intracellular changes that may help facilitate early AD-like neurofibrillary pathology.
<list list-type="bullet"><title>Highlights</title>
<list-item><p><italic>Enterococcus faecalis</italic>
used in the generation of AD neurofibrillary epitopes in rat.</p>
</list-item>
<list-item><p>Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression.</p>
</list-item>
<list-item><p>Infection by <italic>Enterococcus</italic>
may play a role in early Alzheimer neurofibrillary changes.</p>
</list-item>
</list>
</p>
</div>
</front>
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