Abstract
Alzheimer's disease (AD), a neurological disorder, despite significant
advances in medical science, has not yet been definitively cured, and the exact causes
of the disease remain unclear. Due to the importance of AD in the clinic, large expenses
are spent annually to deal with this neurological disorder, and neurologists warn of an
increase in this disease in elderly in the near future. It has been believed that microbiota
dysbiosis leads to Alzheimer’s as a multi-step disease. In this regard, the presence of
footprints of perturbations in the oral microbiome and the predominance of pathogenic
bacteria and their effect on the nervous system, especially AD, is a very interesting topic
that has been considered by researchers in the last decade. Some studies have looked
at the mechanisms by which oral microbiota cause AD. However, many aspects of this
interaction are still unclear as to how oral microbiota composition can contribute to this
disease. Understanding this interaction requires extensive collaboration by
interdisciplinary researchers to explore all aspects of the issue. In order to reveal the
link between the composition of the oral microbiota and this disease, researchers from
various domains have sought to explain the mechanisms of shift in oral microbiota in AD
in this review.
Keywords:
Oral microbiome, Alzheimer's disease, gut microbiota, dysbiosis, periodontitis, microbial.
[4]
Łanowy P, Bichalski M, Komasa J, Mocny-Pachońska K, Tanasiewicz M. Oral microbiota and systemic disease. J Educ Health Sport 2019; 9(8): 811-22.
[8]
Sampaio-Maia B, Caldas I, Pereira M, Perez-Mongiovi D, Araujo R. The oral microbiome in health and its implication in oral and systemic diseases. Advances in applied microbiology 97. Elsevier 2016; pp. 171-210.
[15]
Leblhuber F, Huemer J, Steiner K, Gostner JM, Fuchs D. Knock-on effect of periodontitis to the pathogenesis of Alzheimer’s disease? Wien Klin Wochenschr 2020; 132(17-18): 493-8.
[69]
World Health Organization. Global action plan on the public health response to dementia 2017–2025.
[82]
Glabe CC. Amyloid accumulation and pathogensis of Alzheimer’s disease: Significance of monomeric, oligomeric and fibrillar A β Alzheimer’ s Disease. Springer 2005; pp. 167-77.
[90]
Alcolea-Palafox M, Posada-Moreno P, Ortuño-Soriano I, et al. Research strategies developed for the treatment of Alzheimer’s disease. Reversible and pseudo-irreversible inhibitors of acetylcholinesterase: Structure-activity relationships and drug design. Drug Design and Discovery in Alzheimer’s Disease. Elsevier 2014; pp. 426-77.
[101]
Na HS, Jung NY, Choi S, et al. Analysis of oral microbiome in chronic periodontitis with Alzheimer’s disease: Pilot study.Res Square. 2020; p. 2020.
[103]
Siddiqui H, Eribe ER, Singhrao SK, Olsen I. High throughput sequencing detect gingivitis and periodontal oral bacteria in Alzheimer’s disease autopsy brains. J Neurosci Res 2019; 1(3)
[104]
Leblhuber F, Huemer J, Steiner K, Fuchs D. On the potential role of periodontitis in the pathogenesis of Alzheimer’s. Acta Microbiol Bulg 2020; 132(17-18): 493-8.
[113]
Soscia S, Kirby J, Washicosky K, Tucker S, Ingelsson M. The Alzheimer’s disease-associated amyloid b-protein is an antimicrobial. PloS One 2010; 5(3): e9505.
[118]
Olsen I. Possible link between Porphyromonas gingivalis and amyloidosis in the pathogenesis of Alzheimer’s and Parkinson’s disease. Int J Pathol 2020; 1(1): 1-12.