학술논문

Association of periodontitis with cognitive decline and its progression: Contribution of blood‐based biomarkers of Alzheimer's disease to this relationship.
Document Type
Article
Source
Journal of Clinical Periodontology. Nov2023, Vol. 50 Issue 11, p1444-1454. 11p.
Subject
*DISEASE progression
*BIOMARKERS
*HYPERTENSION
*ALZHEIMER'S disease
*CONFIDENCE intervals
*PERIODONTITIS
*TAU proteins
*REGRESSION analysis
*AMYLOID beta-protein precursor
*NEUROPSYCHOLOGICAL tests
*PSYCHOLOGICAL tests
*GENE expression
*AMBULATORY blood pressure monitoring
*DESCRIPTIVE statistics
*RESEARCH funding
*COGNITION disorders in old age
*LOGISTIC regression analysis
*SECONDARY analysis
*PROPORTIONAL hazards models
*DISEASE complications
*OLD age
Language
ISSN
0303-6979
Abstract
Aim: To assess whether periodontitis is associated with cognitive decline and its progression as well as with certain blood‐based markers of Alzheimer's disease. Materials and Methods: Data from a 2‐year follow‐up prospective cohort study (n = 101) was analysed. Participants with a previous history of hypertension and aged ≥60 years were included in the analysis. All of them received a full‐mouth periodontal examination and cognitive function assessments (Addenbrooke's Cognitive Examination (ACE) and Mini‐Mental State Examination [MMSE]). Plasma levels of amyloid beta (Aβ)1‐40, Aβ1‐42, phosphorylated and total Tau (p‐Tau and t‐Tau) were determined at baseline, 12 and 24 months. Results: Periodontitis was associated with poor cognitive performance (MMSE: β = −1.5 [0.6]) and progression of cognitive impairment (hazard ratio [HR] = 1.8; 95% confidence interval: 1.0–3.1). Subjects with periodontitis showed greater baseline levels of p‐Tau (1.6 [0.7] vs. 1.2 [0.2] pg/mL, p <.001) and Aβ1‐40 (242.1 [77.3] vs. 208.2 [73.8] pg/mL, p =.036) compared with those without periodontitis. Concentrations of the latter protein also increased over time only in the periodontitis group (p =.005). Conclusions: Periodontitis is associated with cognitive decline and its progression in elderly patients with a previous history of hypertension. Overexpression of p‐Tau and Aβ1‐40 may play a role in this association. [ABSTRACT FROM AUTHOR]