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Neurobiol Aging ; 36(2): 627-33, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25491073

RESUMO

The accumulation of amyloid-ß (Aß) 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 Aß 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 Aß 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 Aß vulnerable brain regions (p = 0.002). We show for the first time in humans an association between periodontal disease and brain Aß load. These data are consistent with the previous animal studies showing that peripheral inflammation/infections are sufficient to produce brain Aß accumulations.


Assuntos
Peptídeos beta-Amiloides/metabolismo , Encéfalo/metabolismo , Doenças Periodontais/metabolismo , Idoso , Doença de Alzheimer/etiologia , Compostos de Anilina , Animais , Encéfalo/diagnóstico por imagem , Radioisótopos de Carbono , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doenças Periodontais/complicações , Fenantrolinas , Tomografia por Emissão de Pósitrons , Compostos Radiofarmacêuticos , Análise de Regressão , Tiazóis
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