Abstract
Background
Selenoprotein P (SELENOP) is a transporter for selenium and has been shown to protect selenium status maintenance in brain against deficiency, supporting neuronal development, neurogenesis and neurocognitive function. Selenium deficiency has previously been associated with cognitive impairment in various populations, but no studies have been carried out in subjects with heart failure (HF).
Purpose
To explore if SELENOP deficiency in subjects with acute HF is associated with cognitive impairment.
Methods
Plasma SELENOP measured through an immunoassay analysis is a well-validated marker of plasma selenium status with the benefit of providing information on the bioavailable fraction of selenium to preferentially supplied cells equipped with receptors for SELENOP uptake. SELENOP was measured in 320 subjects hospitalized for HF. One-hundred-eighty-seven of the subjects also underwent four cognitive tests assessing global cognitive function [Montreal Cognitive Assessment (MoCA)], information processing [Symbol Digit Modalities Test (SDMT)], visual attention and task switching [Trailmaking Test A (TMT-A)], and executive speed [A Quick Test of Cognitive Speed (AQT) form and color]. Appropriate cut-offs were used for each cognitive test to define cognitive impairment. Cross-sectional associations between SELENOP concentrations and cognitive impairment defined by each cognitive test were explored using multivariable logistic models. Further, multivariable logistic models exploring associations between selenium deficiency defined as the lowest quartile of SELENOP levels and cognitive impairment defined by each cognitive test were carried out.
Results
The 187 participants had a mean age 73 (±11.9) years; 31% were female, with a mean BMI of 28.1 (±5.6) kg/m2. Each 1 SD increment in SELENOP-concentrations was associated with lower odds of cognitive impairment defined as MoCA cut-off score <23 (odds ratio (OR) 0.60; 95%CI 0.40-0.91; p= 0.017). Further, SELENOP-concentrations within the lowest quartile (≤2.3 mg/L) were associated with cognitive impairment measured by MoCA (OR 3.10; 95%CI 1.38-6.97; p=0.006), SDMT (OR 2.26; 95%CI 1.10-4.67; p=0.027) and TMT-A (OR 3.40; 95%CI 1.47-7.88; p=0.004)), but not by AQT form and color.
Conclusions
In subjects admitted for heart failure, higher SELENOP concentrations were associated with better performance on the MoCA test reflecting global cognition, and SELENOP-deficiency was associated with cognitive impairment as defined by three cognitive tests.
Selenoprotein P (SELENOP) is a transporter for selenium and has been shown to protect selenium status maintenance in brain against deficiency, supporting neuronal development, neurogenesis and neurocognitive function. Selenium deficiency has previously been associated with cognitive impairment in various populations, but no studies have been carried out in subjects with heart failure (HF).
Purpose
To explore if SELENOP deficiency in subjects with acute HF is associated with cognitive impairment.
Methods
Plasma SELENOP measured through an immunoassay analysis is a well-validated marker of plasma selenium status with the benefit of providing information on the bioavailable fraction of selenium to preferentially supplied cells equipped with receptors for SELENOP uptake. SELENOP was measured in 320 subjects hospitalized for HF. One-hundred-eighty-seven of the subjects also underwent four cognitive tests assessing global cognitive function [Montreal Cognitive Assessment (MoCA)], information processing [Symbol Digit Modalities Test (SDMT)], visual attention and task switching [Trailmaking Test A (TMT-A)], and executive speed [A Quick Test of Cognitive Speed (AQT) form and color]. Appropriate cut-offs were used for each cognitive test to define cognitive impairment. Cross-sectional associations between SELENOP concentrations and cognitive impairment defined by each cognitive test were explored using multivariable logistic models. Further, multivariable logistic models exploring associations between selenium deficiency defined as the lowest quartile of SELENOP levels and cognitive impairment defined by each cognitive test were carried out.
Results
The 187 participants had a mean age 73 (±11.9) years; 31% were female, with a mean BMI of 28.1 (±5.6) kg/m2. Each 1 SD increment in SELENOP-concentrations was associated with lower odds of cognitive impairment defined as MoCA cut-off score <23 (odds ratio (OR) 0.60; 95%CI 0.40-0.91; p= 0.017). Further, SELENOP-concentrations within the lowest quartile (≤2.3 mg/L) were associated with cognitive impairment measured by MoCA (OR 3.10; 95%CI 1.38-6.97; p=0.006), SDMT (OR 2.26; 95%CI 1.10-4.67; p=0.027) and TMT-A (OR 3.40; 95%CI 1.47-7.88; p=0.004)), but not by AQT form and color.
Conclusions
In subjects admitted for heart failure, higher SELENOP concentrations were associated with better performance on the MoCA test reflecting global cognition, and SELENOP-deficiency was associated with cognitive impairment as defined by three cognitive tests.
Original language | English |
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Pages (from-to) | 1452-1461 |
Journal | Journal of Cardiac Failure |
Volume | 30 |
Issue number | 11 |
Early online date | 2024 Feb 14 |
DOIs | |
Publication status | Published - 2024 |
Subject classification (UKÄ)
- Neurology