Background: Emerging evidence has linked electrocardiographic parameters with serum adhesion molecules and cognition; however, their interrelationship has not been explored.
Objective: We sought to investigate the associations of ventricular depolarization and repolarization intervals with serum adhesion molecules and cognitive function among rural-dwelling older adults.
Methods: This population-based study engaged 4,886 dementia-free participants (age ≥60 years, 56.2% women) in the baseline examination (March-September 2018) of MIND-China. Of these, serum intercellular and vascular adhesion molecules (ICAM-1 and VCAM-1) were measured in 1591 persons. We used a neuropsychological test battery to assess cognitive function. Resting heart rate, QT, JT intervals, and QRS duration were assessed with electrocardiogram. Data were analyzed using general linear models adjusting for multiple confounders.
Results: Longer JT interval was significantly associated with lower z-scores of global cognition (multivariable-adjusted β= -0.035; 95% confidence interval = -0.055, -0.015), verbal fluency (-0.035; -0.063, -0.007), attention (-0.037; -0.065, -0.010), and executive function (-0.044; -0.072, -0.015), but not with memory function (-0.023; -0.054, 0.009). There were similar association patterns of QT interval with cognitive functions. In the serum biomarker subsample, longer JT and QT intervals remained significantly associated with poorer executive function and higher serum adhesion molecules. We detected statistical interactions of JT interval with adhesion molecules (pinteraction <0.05), such that longer JT interval was significantly associated with a lower executive function z-score only among individuals with higher serum ICAM-1 and VCAM-1.
Conclusion: Longer ventricular depolarization and repolarization intervals are associated with worse cognitive function in older adults and vascular endothelial dysfunction may play a part in the associations.
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http://dx.doi.org/10.3233/JAD-220874 | DOI Listing |
Alzheimers Dement
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National Tsing Hua University, Hsinchu, Taiwan.
Background: Abnormal brain inflammation is an important feature of Alzheimer's disease (AD). Central nervous system (CNS) inflammation is highly related to immune cell activation. Homeostasis of immune cell activity regulation is crucial for CNS autoimmune response.
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December 2024
Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA.
Background: Vascular dysfunction, blood-brain barrier (BBB) dysregulation, and neuroinflammation are thought to participate in Alzheimer`s disease (AD) pathogenesis, though the mechanism is poorly understood. Among pathways of interest, AD pathology appears to affect vascular endothelial growth factor-A (VEGFA) signaling in a bidirectional manner. Higher VEGF levels are thought to have a protective role and slow cognitive decline.
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December 2024
University of Southern California, Los Angeles, CA, USA.
Background: APOE4 carriers exhibit cerebrovascular dysfunction which may contribute to the development of cognitive decline and dementia; however, the mechanisms underlying this pathophysiology remain unknown. Impaired cerebrovascular reactivity (CVR) may be associated with vascular injury, inflammation, and endothelial dysfunction. To examine whether these processes may be involved in CVR deficits in APOE4 carriers, we explored whether plasma levels of vascular injury markers indicative of inflammation and endothelial dysfunction are associated with impaired CVR to hypercapnia and hypocapnia in older APOE4 carriers.
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February 2025
National Clinical Research Center for Geriatric Disorders, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Furong Laboratory, Changsha, Hunan 410008, P.R. China.
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