Can oral infection be a risk factor for Alzheimer’s disease?

[Gert van der Hoek]

There’s emerging evidence that Alzheimer’s disease may be associated with manifold elevations of number and diversity of periodontal pathogens in the brain.

The scientists researching this field are intrigued by the order of symptoms often seen in AD, which appear consistent with the route an oral pathogen would traverse to enter via the olfactory bulbs. The risk-elevating APOE4 polymorphism has been reported to increase blood-brain barrier permeability, and it is being suggested that amyloid may be an attempted anti-microbial defense.

Ian Spreadbury



Can oral infection be a risk factor for Alzheimer’s disease?

Ingar Olsen and Sim K. Singhrao

Journal of Oral Microbiology 2015, 7: 29143 - 17 September 2015

ABSTRACT

Alzheimer’s disease (AD) is a scourge of longevity that will drain enormous resources from public health budgets in the future. Currently, there is no diagnostic biomarker and/or treatment for this most common form of dementia in humans. AD can be of early familial-onset or sporadic with a late-onset. Apart from the two main hallmarks, amyloid-beta and neurofibrillary tangles, inflammation is a characteristic feature of AD neuropathology. Inflammation may be caused by a local central nervous system insult and/or by peripheral infections.

Numerous microorganisms are suspected in AD brains ranging from bacteria (mainly oral and non-oral Treponema species), viruses (herpes simplex type I), and yeasts (Candida species). A causal relationship between periodontal pathogens and non-oral Treponema species of bacteria has been proposed via the amyloid-beta and inflammatory links.

Periodontitis constitutes a peripheral oral infection that can provide the brain with intact bacteria and virulence factors and inflammatory mediators due to daily, transient bacteremias. If and when genetic risk factors meet environmental risk factors in the brain, disease is expressed, in which neurocognition may be impacted, leading to the development of dementia.

To achieve the goal of finding a diagnostic biomarker and possible prophylactic treatment for AD, there is an initial need to solve the etiological puzzle contributing to its pathogenesis. This review therefore addresses oral infection as the plausible etiology of late-onset AD (LOAD).

LINK TO FULL ARTICLE


Oral infections seem to be associated with a modern, Western diet including flour and sugar, see:

Sequencing ancient calcified dental plaque shows changes in oral microbiota with dietary shifts of the Neolithic and Industrial revolutions