Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes

Judith Miklossy*, Andras Kis, Alexandra Radenovic, Lisa Miller, Laszlo Forro, Ralph Martins, Krzysztof Reiss, Nune Darbinian, Pushpa Darekar, Laszlo Mihaly, Kamel Khalili

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

171 Citations (Scopus)


The pathological hallmarks of Alzheimer's disease (AD) consist of β-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of β-amyloid presursor protein (AβPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced.

Original languageEnglish
Pages (from-to)228-236
Number of pages9
JournalNeurobiology of Aging
Issue number2
Publication statusPublished - Feb 2006
Externally publishedYes


  • Alzheimer's disease
  • Amyloid precursor protein
  • Granulovacuolar degeneration
  • Hyperphosphorylated tau
  • Neurofibrillary tangles


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