An Association of Pathogens and Biofilms with Alzheimer’s Disease

Abstract

As one of the leading causes of dementia, Alzheimer’s disease (AD) is a condition in which individuals experience progressive cognitive decline. Although it is known that beta-amyloid (Aβ) deposits and neurofibrillary tangles (NFT) of tau fibrils are hallmark characteristics of AD, the exact causes of these pathologies are still mostly unknown. Evidence that infectious diseases may cause AD pathology has been accumulating for decades. The association between microbial pathogens and AD is widely studied, and there are noticeable correlations between some bacterial species and AD pathologies, especially spirochetes and some of the oral microbes. Borrelia burgdorferi has been seen to correlate with Aβ plaques and NFTs in infected cells. Because of the evidence of spirochetes in AD patients, Treponema pallidum and other oral treponemes are speculated to be a potential cause of AD. T. pallidum has been seen to form aggregates in the brain when the disease disseminates to the brain that closely resemble the Aβ plaques of AD patients. This review examines the evidence as to whether pathogens could be the cause of AD and its pathology. It offers novel speculations that treponemes may be able to induce or correlate with Alzheimer’s disease.

In silico SNP prediction of selected protein orthologues in insect models for Alzheimer's, Parkinson's, and Huntington’s diseases

“…According to our study, it showed a high protein identity to human with reasonable query coverage in MAPT, ATP13A2, GIGYF2 and RAC1. In addition, its larvae can cultivate Bacteria such as Borrelia burgdorferi 61 , Enterococcus faecalis 62 , and Staphylococcus aureus 63 , which are believed to play a role in neuroinflammation and may contribute to AD.…”

Immune-mediated hematological disease in dogs is associated with alterations of the fecal microbiota: a pilot study

“…in diseased dogs in the current study is a novel finding. Although this spirochete genus has been associated with syphilis [ 59 ], gastritis [ 60 ], Alzheimer’s disease [ 61 ], periodontitis and gingivitis [ 62 ] in people, and periodontitis in dogs [ 63 – 65 ], the potentially protective role of certain Treponema spp. has been poorly characterized.…”

SARS-CoV-2 Neuroinvasion, Inflammatory Neurodegeneration and Alzheimer's Disease

“…Emerging evidence indicates that both DNA and RNA viruses, such as the human double-stranded DNA (dsDNA) Herpes simplex type 1 and 2 (HSV-1, HSV-2), the human cytomegalovirus (HMCV), the Epstein-Barr virus (EBV), and the ssRNA viruses hepatitis C virus (HCV; Herpesviridae), human influenza A viruses (H1N1/H3N2; Orthomyxoviridae), Zika virus (ZIKVs; Flaviviridae), MERS-CoV (Coronaviridae), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; Coronaviridae) and a remarkably large number of bacteria of the genus Bacteroides, Borrelia, Chlamydia, Treponema, Porphyromonas, Prevotella, Tannerella, Fusobacterium, Aggregatibacter, Eikenella and Helicobacter, as well as several other eukaryotic parasites (e.g., Toxicara; Toxoplasma) or fungi (Aspergillus; Candida) and others have been implicated in the etiopathology of inflammatory neurodegenerative diseases including AD. There is also evidence that a syntrophic consortium of complex microorganisms together, known as biofilms, may be involved and additionally contribute to the neuropathology of AD, however the combination of SARS-CoV-2 invasion with other microbes has not been well studied (Chakravarthi and Joshi, 2021;Piekut et al, 2022;Protto et al, 2022). Importantly, all microbial infections of nervous tissues as described above contribute to the development of a microbialor viral-induced cytokine storm, a smoldering and progressive inflammatory neurodegeneration and the appearance of neurofibrillary tangles (NFT), amyloid aggregation and related amyloidogenic processes as are observed during the course of AD (Ball et al, 2013;Hosseini et al, 2021; Chidambaram et al, 2022;Chiner-Vives et al, 2022;Visco et al, 2022).…”