Porphyromonas Gingivalis as a Risk Factor to Alzheimer’s Disease: A Systematic Review

  • Abdelrahman Elwishahy
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany
  • Khatia Antia
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany
  • Sneha Bhusari
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany
  • Nkorika Chiamaka Ilechukwu
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany
  • Olaf Horstick
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany
  • Volker Winkler
    Heidelberg Institute of Global Health, Heidelberg University Hospital, Heidelberg, Germany

Description

<jats:p>Background: Alzheimer’s disease (AD) is a chronic neurodegenerative disease that accounts for more than 50% of all dementia cases worldwide. There is wide consensus on the risk factors of AD; however, a clear etiology remains unknown. Evidence suggests that the inflammatory-mediated disease model, such as that found with periodontal disease due to Porphyromonas gingivalis (P. gingivalis), plays a role in AD progression. Objective: This study aims to systematically review the literature on the association between P. gingivalis to AD, and to identify the homogeneity of the methods used across studies to measure P. gingivalis involvement in AD. Methods: We systematically searched studies on Cochrane library, Ovid Medline, PubMed, Web of Science, WHOLIS, Google Scholar databases, and reference lists of identified studies. Results: 6 studies out of 636 identified records fulfilled all eligibility criteria. Results showed no clear pathophysiology of AD due to P. gingivalis and its various virulence factors. No consensus was found in the literature pertaining to the method of measurement of AD or P. gingivalis and its virulence factors. Conclusion: The included studies suggest that P. gingivalis bacteria play a role in the process of systemic inflammation which leads to cerebrospinal fluid inflammation and indirectly cause hastening of AD onset and progression. Our included studies revealed heterogeneity in the methodologies of measurement of AD and/or P. gingivalis and its virulence factors, which opens discussion about the benefits and weakness of possible standardization.</jats:p>

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