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Related Experiment Videos

Flavio Pisani1, Valerio Pisani2, Francesca Arcangeli3

  • 1Faculty of Clinical and Biomedical Sciences, School of Dentistry, University of Central Lancashire, Preston PR1 2HE, UK.

International Journal of Environmental Research and Public Health
|June 10, 2023
PubMed
Summary

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This review explores the hypothesis that the bacterium Treponema denticola may initiate Alzheimer's disease (AD) pathology by damaging peripheral nerves and evading immune responses, potentially leading to neurodegeneration.

Area of Science:

  • Neuroscience
  • Microbiology
  • Pathology

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, characterized by amyloid-beta plaques and tau tangles.
  • Traditional AD progression models focus on cortical spread, but emerging evidence suggests a potential midbrain origin.
  • Spirochetes are known to be neurotrophic, capable of reaching the brain via the midbrain.

Purpose of the Study:

  • To review the hypothesis that Treponema denticola contributes to Alzheimer's disease pathogenesis.
  • To explore the mechanisms by which T. denticola might cause axonal damage, immune evasion, and neuronal apoptosis.
  • To propose a pathogenetic model for advanced AD involving T. denticola.

Main Methods:

  • Review of existing literature on T. denticola, neurodegeneration, and immune responses.
Keywords:
Alzheimer’s diseaseTreponema denticolaaxonal transportcytoskeletal impairmentmitochondrial dockingneurodegenerationperiodontal diseaseperipheral nerve

Related Experiment Videos

  • Analysis of spirochete virulence factors and their interaction with host cells like microglia.
  • Discussion of biofilm formation and quorum sensing in T. denticola's immune resistance.
  • Main Results:

    • T. denticola may damage peripheral axons and evade immune responses, including complement and microglial activity.
    • Bacterial virulence factors can lead to cytoskeletal impairment, disrupted axonal transport, and altered mitochondrial function.
    • These disruptions can result in neuronal apoptosis, potentially contributing to AD progression.

    Conclusions:

    • Treponema denticola is proposed as a potential etiological agent in Alzheimer's disease, particularly in advanced stages.
    • The bacterium's ability to damage peripheral nerves and evade immunity offers a novel perspective on AD pathogenesis.
    • Further research into T. denticola's role, especially its biofilm and quorum sensing mechanisms, is warranted to understand its central neurodegeneration pathways.