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Neurobiol Aging. 2015 Feb;36(2):627-33. doi: 10.1016/j.neurobiolaging.2014.10.038. Epub 2014 Nov 5.

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

Author information

1
Department of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA; School of Medicine, Department of Psychiatry, Center for Brain Health, New York, NY, USA. Electronic address: ark5@nyu.edu.
2
School of Medicine, Department of Psychiatry, Center for Brain Health, New York, NY, USA.
3
School of Medicine, Department of Psychiatry, Center for Brain Health, New York, NY, USA; School of Medicine, Department of Radiology, New York, NY, USA.
4
Weill Medical Center, Department of Radiology, Cornell University, New York, NY, USA.
5
Department of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA; Department of Basic Sciences and Craniofacial Biology, College of Dentistry, New York University, New York, NY, USA.
6
Department of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA.
7
Department of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA; College of Dentistry, Bluestone Center for Clinical Research, New York University, New York, NY, USA.
8
Department of Basic Sciences and Craniofacial Biology, College of Dentistry, New York University, New York, NY, USA.

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.

KEYWORDS:

Alzheimer's disease; Brain amyloid; Cognition; Infection; Inflammation; PIB-PET; Periodontal disease

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