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, 36 (2), 627-33

Periodontal Disease Associates With Higher Brain Amyloid Load in Normal Elderly

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Periodontal Disease Associates With Higher Brain Amyloid Load in Normal Elderly

Angela R Kamer et al. Neurobiol Aging.

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.

Conflict of interest statement

Conflict of interest: No conflict of interest is reported for A. Kamer, P. Corby, R. Craig, D. Saxena, H. Rusinek, S. Vallabhajosula, S. Williams, R. Linker, S. Svetco and C. Shi. L. Mosconi, W. Tsui, and M. de Leon have a patent on an image analysis technology that was licensed to Abiant Imaging, Inc, by NYU, and have a financial interest in this license agreement, and NYU holds stock options on the company. Y. Li, L. Mosconi and M. de Leon have received compensation for consulting services from Abiant Imaging. Dr L. Glodzic was a Principal Investigator on an Investigator-Initiated project funded by Forest Laboratories, Inc, and received an honorarium for serving as a consultant to Roche Pharma.

Figures

Figure 1
Figure 1
Partial regression plots show the relationships between CAL3 (A) and CAL4 (B) and PIB retention in MaskAD. The x and y axes are the residuals for CAL3 and CAL4 respectively and PIB retention adjusted for age, ApoE carrier status and smoking. The changes in R2 (ΔR2) and p values for these changes are shown. MaskAD is defined by combining the standardized uptake value ratios (SUVR) of inferior parietal lobule, lateral temporal lobe, middle frontal gyrus, posterior cingulate cortex/precuneus, and prefrontal cortex. Note, the CAL3-SUVR and CAL4-SUVR associations are significant.
Figure 2
Figure 2
PIB-PET scans of four representative NL individuals: two of them age 72 and 75 are ApoE carriers with high CAL3 (A) and low CAL3 (C) and two of them age 79 and 76 are ApoE non-carriers with high CAL3 (B) and low CAL3 (D). Note: the subjects in the upper row have significant amyloid accumulation and high CAL3 measures while the subjects in the lower row have low brain amyloid accumulation and low CAL3. PIB-PET scans for each subject are displayed as axial sections encompassing basal ganglia (first slide) and inferior parietal level (second slide) respectively. PIB measures are standardized uptake value ratios (SUVR) to cerebellar gray matter. Note: the APOE4-positive subject presents with a positive PIB pattern while the APOE4-negative subject presents with an “emerging PIB pattern” in the right temporal-occipital cortex. A. PIB positive e4 carrier; B. PIB positive e4 non-carrier; C. PIB negative e4 carrier; D. PIB negative e4 non-carrier.

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