Periodontal disease associates with higher brain amyloid load in normal elderly.

Publication Type	Academic Article
Authors	Kamer A, Pirraglia E, Tsui W, Rusinek H, Vallabhajosula S, Mosconi L, Yi L, McHugh P, Craig R, Svetcov S, Linker R, Shi C, Glodzik L, Williams S, Corby P, Saxena D, de Leon M
Journal	Neurobiol Aging
Volume	36
Issue	2
Pagination	627-33
Date Published	11/05/2014
ISSN	1558-1497
Keywords	Amyloid beta-Peptides, Brain, Periodontal Diseases
Abstract	The accumulation of amyloid-β (Aβ) plaques is a central feature of Alzheimer's disease (AD). First reported in animal models, it remains uncertain if peripheral inflammatory and/or infectious conditions in humans can promote Aβ brain accumulation. Periodontal disease, a common chronic infection, has been previously reported to be associated with AD. Thirty-eight cognitively normal, healthy, and community-residing elderly (mean age, 61 and 68% female) were examined in an Alzheimer's Disease Research Center and a University-Based Dental School. Linear regression models (adjusted for age, apolipoprotein E, and smoking) were used to test the hypothesis that periodontal disease assessed by clinical attachment loss was associated with brain Aβ load using (11)C-Pittsburgh compound B (PIB) positron emission tomography imaging. After adjusting for confounders, clinical attachment loss (≥3 mm), representing a history of periodontal inflammatory/infectious burden, was associated with increased PIB uptake in Aβ vulnerable brain regions (p = 0.002). We show for the first time in humans an association between periodontal disease and brain Aβ load. These data are consistent with the previous animal studies showing that peripheral inflammation/infections are sufficient to produce brain Aβ accumulations.
DOI	10.1016/j.neurobiolaging.2014.10.038
PubMed ID	25491073
PubMed Central ID	PMC4399973