Background: Beta amyloid (Aβ) peptide containing plaque aggregations in the brain are a
hallmark of Alzheimer’s Disease (AD). However, Aβ is produced by cell types outside of the brain
suggesting that the peptide may serve a broad physiologic purpose.
Objective: Based upon our prior work documenting expression of amyloid β precursor protein (APP)
in intestinal epithelium we hypothesized that salivary epithelium might also express APP and be a
source of Aβ.
Methods: To begin testing this idea, we compared human age-matched control and AD salivary glands
to C57BL/6 wild type, AppNL-G-F
, and APP/PS1 mice.
Results: Both male and female AD, AppNL-G-F
, and APP/PS1 glands demonstrated robust APP and Aβ
immunoreactivity. Female AppNL-G-F mice had significantly higher levels of pilocarpine stimulated Aβ
1-42 compared to both wild type and APP/PS1 mice. No differences in male salivary Aβ levels were
detected. No significant differences in total pilocarpine stimulated saliva volumes were observed in
any group. Both male and female AppNL-G-F but not APP/PS1 mice demonstrated significant differences
in oral microbiome phylum and genus abundance compared to wild type mice. Male, but not female,
APP/PS1 and AppNL-G-F
mice had significantly thinner molar enamel compared to their wild type counterparts.
Conclusion: These data support the idea that oral microbiome changes exist during AD in addition to
changes in salivary Aβ and oral health.