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Inflammation and Alzheimer's Disease: Possible Role Of Alzheimer’s & Dementia 4 (2008) 242–250 Inflammation and Alzheimer’s disease: Possible role of periodontal diseases Angela R. Kamera,*, Ronald G. Craiga,b, Ananda P. Dasanayakec, Miroslaw Brysd, Lidia Glodzik-Sobanskad, Mony J. de Leond,e aDepartment of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA bDepartment of Basic Sciences and Craniofacial Biology, College of Dentistry, New York University, New York, NY, USA cDepartment of Epidemiology and Health Promotion, College of Dentistry, New York University, New York, NY, USA dDepartment of Psychiatry, School of Medicine, New York University, New York, NY, USA eNathan Kline Institute, Orangeburg, NY, USA Abstract The molecular and cellular mechanisms responsible for the etiology and pathogenesis of Alzheimer’s disease (AD) have not been defined; however, inflammation within the brain is thought to play a pivotal role. Studies suggest that peripheral infection/inflammation might affect the inflammatory state of the central nervous system. Chronic periodontitis is a prevalent peripheral infection that is associated with gram-negative anaerobic bacteria and the elevation of serum inflammatory markers including C-reactive protein. Recently, chronic periodontitis has been asso- ciated with several systemic diseases including AD. In this article we review the pathogenesis of chronic periodontitis and the role of inflammation in AD. In addition, we propose several potential mechanisms through which chronic periodontitis can possibly contribute to the clinical onset and progression of AD. Because chronic periodontitis is a treatable infection, it might be a readily modifiable risk factor for AD. © 2008 The Alzheimer’s Association. All rights reserved. Keywords: Alzheimer’s disease; Inflammation; Periodontitis; Pathogenesis model 1. Introduction crease unless new approaches to treatment emerge that can delay the onset, slow the progression, or reverse the Alzheimer’s disease (AD) is one of the leading causes of disease process. Efforts to identify treatable factors in- dementia afflicting the elderly. In the United States, approx- volved in the initiation and progression of AD are there- imately 4.5 million patients are currently diagnosed with AD. The prevalence of AD increases with age from 4% in fore of paramount importance. the 65 to 75 years age group to 19% in the 85 to 89 years Early onset AD is thought to be genetically deter- age group, and the incidence of AD increases from mined, whereas late onset or sporadic AD, which in- 7/1000 in the 65 to 69 years age group to 118/1000 in the cludes the majority of patients, is believed to result from 85 to 89 years age group. Undoubtedly, as the population the interaction of genetic and environmental factors. Age ages and life span increases, the prevalence of AD will is a significant risk factor for AD. Other risk factors for increase even further and in 50 years is predicted to late onset AD identified to date include family history, include approximately 14 million people. Although the education, high fat diet, hypertension, diabetes, history of above statistics underscore AD as a major public health head trauma, and susceptibility genes such as APOE. concern, the prevalence of AD will not significantly de- Among them, age, family history, and APOE ␧4 allele are accepted risk factors. The others are possible and are still *Corresponding author. Tel.: 212-998-9868; fax: 212-995-4603. being investigated. Table 1 presents odds ratios for se- E-mail address: [email protected] lected risk factors. 1552-5260/08/$ – see front matter © 2008 The Alzheimer’s Association. All rights reserved. doi:10.1016/j.jalz.2007.08.004 A.R. Kamer et al. / Alzheimer’s & Dementia 4 (2008) 242–250 243 Table 1 2. The association of inflammation with AD Risk Factors for AD Risk factor Odds ratio Source 2.1. Inflammatory mechanisms in AD Family history of AD 4.6–6.6 Hall et al,1 1998, Brayne et al,2 A prominent hypothesis forwarded to explain the patho- or dementia 1998 genesis of AD is the inflammatory hypothesis [2], whose 3 ApoE 4 at least 1 allele 2.6–4.6 Farrer et al, 1997 central theme is a self-perpetuating progressive inflamma- Hyperhomocystinemia 3.7–4.5 Clarke et al,4 1998, Quadri et al,5 2004 tion in the brain culminating in neurodegeneration. At Head trauma 1.1–3.6 Fleminger et al,6 2003 (review) present, no local inciting inflammatory factors for AD are Severe atherosclerosis 3.0 Hofman et al,7 1997 accepted. It has been suggested that inflammation might be Smoking 2.4 Tyas et al,8 2003 induced by the pathologic features of AD, including A␤- 9 Hypertension 2.3 Kivipelto et al, 2001 amyloid 1-42 peptide (A␤42) found in senile plaques, hy- Hyperlipidemia 2.1 Kivipelto et al,9 2001 Depression 1.7–1.8 Andersen et al,10 2005, Speck perphosphorylated tau protein (P-Tau) comprising the neu- et al,11 1995 rofibrillary tangles, or components of degenerated neurons Diabetes 1.4 Brayne et al,2 1998 [3]. These pathologic changes are believed to stimulate glial NOTE. Odd ratios for AD risk factors are presented. Family history and cells to produce proinflammatory cytokines including tumor APOE with an e4 allele are accepted risk factors. The other risk factors are necrosis factor (TNF)–␣, interleukin (IL)-1␤, IL-6, and in- possible and are being investigated. References are also given. These flammation reactive proteins such as C-reactive protein references are different from those references cited in the text. (CRP). Elevated proinflammatory cytokines and CRP might 1 Hall K, Gureje O, Gao S, Ogunniyi AO, Hui SL, Baiyewu. Aus New Zealand J Psych 1998;32:698–706. then act via paracrine and/or autocrine pathways to stimu- 2 Brayne C, Gill C, Huppert FA, Gehlhaar E, Girling DM, O’Connor late glial cells to further produce additional A␤42, P-Tau, DW. Dement Geriatr Cogn Disord 1998;9:175–80. and proinflammatory molecules. Thus, a positively reinforc- 3 Farrer LA, Cuples LA, Haines JL, Hyman B, Kukull WA, Mayeux R. ing cycle is established in which inflammatory mediators JAMA 1997;278:1349–56. play a dual role by both stimulating glial cells and activating 4 Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, Ueland PM. Arch Neurol 1998;55:1449–55. molecular pathways, leading to neurodegeneration [2]. Sev- 5 Quadri P, Fragiacomo C, Pezzati R, Zanda E, Forloni G, Tettamanti M. eral lines of evidence support this model. Senile plaques are Am J Clin Nutr 2004;80:114–22. associated with reactive astrocytes and activated microglial 6 Fleminger S, Oliver DL, Lovestone S, Rabe-Hesketh S, Giora A. cells [3] and immunoreact with antibodies against TNF-␣, J Neurol Neurosurg Psychiatry 2003;74:857–62. 7 IL-1␤, IL-6, CRP, and complement proteins [3]. TNF-␣, Hofman A, Ott A, Breteler MMB, Bots ML, Slooter AJC, van Har- ␤ skamp F. Lancet 1997;349:151–4. IL-1 , and IL-6 are capable of stimulating the synthesis of 8 Tyas SL, White LR, Petrovitch H, Webster Ross G, Foley DJ, Heimo- A␤42 and the phosphorylation of tau protein, and A␤42 and vitz HK. Neurobiol Aging 2003;24:589–96. P-Tau can stimulate the production of TNF-␣, IL-1␤, and 9 Kivipelto M, Helkala EL, Hanninen T, Laakso MP, Hallikainen M, IL-6 by glial cells [2–5]. Alhainen K. Neurology 2001;56:1683–9. 10 Andersen K, Lolk A, Kragh-Sorensen P, Petersen NE, Green A. Clinical studies in support of the role of inflammation in Epidemiology 2005;16:233–8. the pathogenesis of AD, although limited, have investigated 11 Speck CE, Kukull WA, Brenner DE, Bowen JD, McCormick WC, the value of CRP (an acute phase protein whose synthesis is Teri L. Epidemiology 1995;6:366–9. regulated by proinflammatory cytokines in response to in- fection/inflammation) and other systemic inflammatory Some of the above risk factors for AD are immutable, but markers in predicting the onset of AD. Elevated CRP in- the identification of modifiable risk factors might hold the creased the risk of both developing AD [6] and of cognitive potential for intervention, thus limiting the prevalence and decline in various populations [7]. A nested case-control morbidity of AD in the future. Although the molecular study of 1,050 subjects from the Honolulu-Asia Aging mechanisms involved in the etiology and pathogenesis of Study reported that higher levels of CRP increased the risk AD have not been completely characterized, inflamma- of developing AD 25 years later [8]. Proinflammatory cy- tion within the central nervous system (CNS) is thought tokines as predictors of AD have also been investigated, to play a pivotal role. Central to the role of inflammation however with conflicting results. For example, elevated in AD is the hypothesis that peripheral infection/inflam- IL-6 moderately increased the risk of AD, even after ad- mation might alter the inflammatory state in the brain. justing for age, gender, smoking, body mass index, medi- Indeed, preliminary studies have shown that peripheral cations, and diabetes, and correlated with disease severity infections might hasten the onset and progression of AD [9]. AD subjects with elevated IL-1␤ were at increased risk [1], although the specific mechanisms and pathways in- of cognitive decline compared with those with low IL-1␤ volved have not been defined. The intent of this article is [10], whereas the presence of a composite genotype char- to review the role of inflammation in the pathogenesis of acterized by the presence of IL-1␣-889 and IL-1␤ϩ3953 AD and suggest the contribution of periodontal disease to polymorphisms conferred an almost 11-fold increased risk the clinical onset and progression of AD.
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