This study is designed to obtain data exploring the role of periodontal disease in the pathogenesis of Alzheimer’s disease. PD is a chronic infection resulting from the interaction of periodontopathic bacteria and a host response. This interaction leads to localized and systemic inflammation characterized by elevation of inflammatory molecules such as IL-1ß, IL-6, IL8, TNF-? ?, CRP; and , high antibodies levels. PD through bacteria and/or inflammatory molecules may contribute to already elevated brain inflammatory molecules, therefore increasing risk of AD. We hypothesize that subjects with periodontal infections will be at an increased risk of developing AD.
Objectives: We will determine whether a greater proportion of subjects developing AD had elevated levels of antibody titers to Aa, Pg, Td and Tf (markers of periodontopathic bacteria) and of systemic inflammatory markers (IL-1ß, Il-6, TNF-? ?, CRP and others) at baseline as compared control subjects. Methods: Stored plasma samples collected at baseline evaluation at the NYU ADCC and the affiliated CBH from cohorts of subjects are used in a nested case-control. Cases (AD) and Controls (NL, MCI) will be compared for the existence of exposures at baseline (antibodies to Aa, Pg, Td, Tf, CRP and cytokines). In this project we characterized the study population using several parameters, such as age, gender and race.
Results: Since cytokine levels may differ based on the year of collection we characterized our study population by year. Our results showed that in 1998, 1999, 2000 and 2001 age was statistically greater in AD subjects compared to controls. In 1997 and 2004 age difference approached statistical significance. In contrast there was no significant difference in gender and race among groups. Conclusion: Our results showed that AD subjects are older than controls subjects suggesting that this parameter has to be considered in the final study analysis.
Akhtar S, Kamer AR. IADR General Session, Miami, FL April 2009.