Low levels of salivary lactoferrin may affect oral dysbiosis and contribute to Alzheimer's disease: A hypothesis

Abstract

Recently it has been reported that reduced levels of salivary lactoferrin (LF) can be a plausible biomarker for amyloid beta (Aβ) accumulation in Alzheimer's disease (AD) brains. This could mean that reduced levels of salivary LF act as a trigger for oral dysbiosis and that low LF levels could change the oral microbiota. A chemical change in the composition of saliva has not yet been considered as a cause for microbial dysbiosis but does present an opportunity to view oral dysbiosis as a plausible contributory factor in the development of AD pathophysiology. Oral dysbiosis has largely been reported as a result of inadequate oral hygiene and dry mouth in elderly subjects. Here we discuss if the deficiency of LF in saliva and gingival fluid of AD patients can facilitate proliferation of oral pathogens, and as a result their spread elsewhere in the body. Additionally, we ask if LF in the AD brain could be overexposed as a result of chronic infection. Together these outcomes will indicate if reduced levels of salivary LF can act as a trigger of oral dysbiosis.

Keywords: Brain; Dysbiosis; Gingipains; Lactoferrin; Porphyromonas gingivalis; Saliva.