Chronic spirochetal infection can cause slowly progressive dementia, cortical
atrophy and amyloid deposition in the atrophic form of general paresis. There is
a significant association between Alzheimer disease (AD) and various types of
spirochete (including the periodontal pathogen Treponemas and Borrelia
burgdorferi), and other pathogens such as Chlamydophyla pneumoniae and herpes
simplex virus type-1 (HSV-1). Exposure of mammalian neuronal and glial cells and
organotypic cultures to spirochetes reproduces the biological and pathological
hallmarks of AD. Senile-plaque-like beta amyloid (Aβ) deposits are also observed
in mice following inhalation of C. pneumoniae in vivo, and Aβ accumulation and
phosphorylation of tau is induced in neurons by HSV-1 in vitro and in vivo.
Specific bacterial ligands, and bacterial and viral DNA and RNA all increase the
expression of proinflammatory molecules, which activates the innate and adaptive
immune systems. Evasion of pathogens from destruction by the host immune
reactions leads to persistent infection, chronic inflammation, neuronal
destruction and Aβ deposition. Aβ has been shown to be a pore-forming
antimicrobial peptide, indicating that Aβ accumulation might be a response to
infection. Global attention and action is needed to support this emerging field
of research because dementia might be prevented by combined antibiotic,
antiviral and anti-inflammatory therapy.
http://www.ncbi.nlm.nih.gov/pubmed/21933454
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