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Resting heart rate (RHR) is a strong predictor of adverse cardiovascular outcomes. Both soluble low-density lipoprotein receptor-related protein-1 (sLRP1) and soluble receptor for advanced glycation end products (sRAGE) are novel plasma biomarkers for atherosclerosis. In this study, we examined the potential associations between RHR and plasma sLRP1 and sRAGE levels and whether any associations might be modified by apolipoprotein E (APOE) ε4 carrier status.This cross-sectional study included 941 apparently healthy adults aged 40 years or older. Plasma sLRP1 and sRAGE levels were measured by a commercial enzyme-linked immunosorbent assay. APOE gene polymorphisms were analyzed by a polymerase chain reaction and Sanger sequencing.RHR was a significant determinant of log-transformed sLRP1 (β = 0.004; 95% confidence interval [CI], 0.002-0.007; P = 0.001) and log-transformed sRAGE (β = 0.005; 95% CI, 0.002-0.007; P0.001) independently of age, sex, body mass index, blood pressure, blood glucose, blood lipids, lifestyle, and medical history. Additionally, APOE ε4 carrier status was inversely associated with log-transformed plasma sLRP1 level (β = -0.072; 95% CI, -0.130 to -0.015; P = 0.01) and did not modify the relationship between RHR and plasma sLRP1 level.An elevated RHR was associated with increased sLRP1 and sRAGE values, which was not modified by APOE genotype. The underlying mechanism of this effect may be relevant to the progression of atherosclerosis.

Background: Abnormal blood lipids are associated with cognitive impairment and amyloid-β (Aβ) deposition in the brain. However, the effects of statins on Alzheimer’s disease (AD) have not been determined. Objective: Considering that plasma Aβ are related to Aβ deposition in the brain, we investigated the effects of simvastatin on plasma Aβ transport. Methods: This was a randomized, double-blind, placebo-controlled trial. One hundred and twenty patients with hyperlipidemia were randomly assigned to receive 40 mg of simvastatin per day or matching placebo for 12 weeks (sixty patients per group). Plasma Aβ, sLRP1, sRAGE, and lipid levels were measured at baseline and at the 6-week and 12-week visits. Results: The ITT database ultimately included 108 participants (placebo group: n = 53; simvastatin group: n = 55) and 64 (59.3%) were women, ranging in age from 45 to 75 years (mean 57.2±6.9 years). Multiple linear regression analysis showed that, after 12 weeks of follow-up, compared with the placebo group, ΔAβ42 levels (the change of Aβ42 levels from baseline at week 12) increased more and ΔsRAGE levels decreased more in the simvastatin group (Aβ42: β= 5.823, p = 0.040; sRAGE: β= –72.012, p = 0.031), and a significant negative association was found between ΔAβ42 and ΔsRAGE levels (β= –0.115, p = 0.045). In addition, generalized estimation equation analysis showed that triglycerides levels were negatively correlated with Aβ40 (β= –16.79, p = 0.023), Aβ42 (β= –6.10, p = 0.001), and sRAGE (β= –51.16, p = 0.003). Conclusion: Daily oral simvastatin (40 mg/day) in patients with hyperlipidemia for 12 weeks can significantly increase plasma Aβ42 levels compared with placebo, which was associated with reduced triglycerides and sRAGE levels, indicating that statins may affect plasma Aβ transport.

Introduction: The relationship between obesity and cognitive impairment (CI) is highly heterogeneous in previous studies, which may be due to insufficient consideration of anthropometric indicators and sex. This study compared the cross-sectional relationships among body mass index (BMI), waist-to-hip ratio (WHR) and CI among people aged ≥40 years, and sex-specific relationships were also considered. Methods: This was a population-based cross-sectional study with a cluster sampling design. CI was defined as a Mini-Mental State Examination score lower than the cutoff value. Multivariate logistic regression was used. BMI and WHR were fitted as both restricted cubic splines and categorical data. Stratified analysis and interaction analysis were performed to explore the sex-specific relationship. Results: A total of 1792 subjects (40.5% male) were analyzed, and 230 were confirmed to have CI. The relationships among BMI, WHR and CI were significant (Poverall=0.023, Pnonlinear=0.097; Poverall=0.017, Pnonlinear=0.078, respectively) but exhibited an opposite trend in the total population in the analyses with BMI and WHR as restricted cubic splines. Further categorical analyses showed that subjects with a BMI 0.92 had a significantly higher risk of CI than those with a WHR ≤0.92 (11.7% vs. 16.2%, P=0.011; OR = 1.619 [1.161–2.258], P = 0.005). In addition, the relationship between a low BMI and CI was more significant in males (P = 0.034), while the relationship between a high WHR and CI was more significant in females (P = 0.002). Further studies is needed to confirm the sex differences because of the marginal significance result in the interaction analysis (P = 0.051 for interaction term BMI×sex; P = 0.056 for interaction term WHR×sex). Discussion/Conclusion: The relationships among BMI, WHR and CI exhibit an opposite trend. A low BMI or high WHR was positively associated with CI, which was more prominent in males for a low BMI, and in females for a high WHR.

Background: Transport proteins, soluble LRP1 (sLRP1) and soluble RAGE (sRAGE), play a pivotal role in the peripheral clearance of plasma amyloid-β (Aβ). However, their relationship is seldom discussed, especially in Alzheimer’s disease (AD). Objective: To explore whether their relationship in patients with AD varied from those in cognitively normal (CN) controls. Methods: We initially recruited 70 patients with AD and 725 CN controls, then applied propensity score matching (PSM) analysis to balance the differences between two groups. Plasma levels of sLRP1, sRAGE, and Aβ were measured using commercial ELISA kits and log transformed when skewed distributed. The relationship between sLRP1/sRAGE and plasma Aβ were analyzed using Pearson’s correlation analysis followed by multiple linear regression separately in the original population and matched participants. Results: After PSM, 70 patients with AD and 140 matched controls were included for further analysis. Log sLRP1 was positively correlated with plasma Aβ40 in matched CN controls (r = 0.222, p = 0.008) but not in patients with AD (r = 0.137, p = 0.260). After multivariable adjustment, Log sLRP1 remained significantly associated with plasma Aβ40 in the CN group (β= 7.347, p = 0.014) but not in the AD group (β= 10.409, p = 0.105). In contrast, Log sLRP1 was not correlated with plasma Aβ42 in patients with AD or CN controls, and Log sRAGE was consistently not associated with plasma Aβ40 or Aβ42 in either group. Conclusion: The significant correlation between sLRP1 and plasma Aβ40 present in CN controls was not found in patients with AD, suggesting that their relationship was different in AD. However, the specific mechanisms and its influence on cerebral amyloid burden require further validation.

Objective The effects of the Apolipoprotein E (ApoE) genotype on peripheral amyloid beta (Aβ) and Aβ transporter levels are still unclear. Soluble low-density lipoprotein receptor-related protein-1 (sLRP1) and soluble receptor of advanced glycation end products (sRAGE) are the major transporter for Aβ, which can prevent plasma Aβ from flowing into brain. The aim of this study was to investigate the relationships between the ApoE genotype and plasma Aβ, sLRP1, sRAGE levels. Design Cross-sectional study. Setting The committee office of the village. Participants Residents lived in the village for more than 3 years, aged 40–85 years (n = 1,119, 63.5% women). Measurements Plasma biomarkers include ApoE genotype, Aβ, sLRP1, sRAGE, fasting blood-glucose, and blood lipids. General information, medical history, living habits, and cognitive status (cognitive impairment or not) were also collected. Results After controlling for all possible covariates, multiple linear regression analysis showed that the plasma level of Aβ42 was higher and log-transformed sLRP1 was lower in ApoE e4 carriers than that in noncarriers (βAβ42 = 1.214, 95% confidence interval: 0.105–2.316, pAβ42 = 0.031; βsLRP1 = −0.075, 95% confidence interval: −0.129 to −0.021, psLRP1 = 0.006, respectively). Partial correlation analysis showed that plasma Aβ40 was positively correlated with log-transformed sLRP1 and log-transformed sRAGE (rsLRP1 = 0.116, psLRP1 Conclusion ApoE e4 carriers had higher plasma Aβ42 levels and lower sLRP1 levels. These data indicated that the ApoE e4 allele may also contribute to the pathogenesis of Alzheimer's disease through its effects on peripheral Aβ42 and sLRP1 levels, but it needs to be further elucidated.

Background: Soluble low-density lipoprotein receptor-related protein-1 (sLRP1) and soluble receptor of advanced glycation end products (sRAGE) play major roles in peripheral clearance of amyloid-β (Aβ). Objective: To determine the relationship between baseline sLRP1/sRAGE and early cognitive decline in a longitudinal study and explore the possible effect of apolipoprotein E (APOE) on their association. Methods: Cognitively normal subjects were followed-up for 4 years. The baseline plasma levels of sLRP1 and sRAGE were measured using commercial ELISA kits. Global cognition was evaluated by Mini-Mental State Examination (MMSE), and cognitive decline was defined as a ≥2-point decrease of MMSE after 4 years. The association between baseline sLRP1/sRAGE and 4-year cognitive decline were analyzed using logistic regression analysis. Interaction analysis was performed to discover the potential effect of APOE genotype on the relationship. Results: 769 participants were included in the final analysis, with 122 subjects (15.86%) were cognitive decline. Baseline sLRP1/sRAGE levels were not associated with 4-year cognitive decline after multivariable adjustments in the total cohort. However, there was significant interaction effect between sRAGE and APOE genotype on cognitive decline (adjusted odds ratio [OR] = 2.09, 95% confidence interval [CI]: 1.13–3.86, p = 0.019). Lower levels of sRAGE were associated with increased risk of cognitive decline among APOE ɛ4 non-carriers (adjusted OR = 1.60, 95% CI: 1.04–2.48, p = 0.034). Conclusion: Individuals with lower levels of sRAGE had an increased risk of 4-year cognitive decline in APOE ɛ4 non-carriers, indicating that the association between sRAGE and cognitive decline might depend on the APOE genotype. However, the specific mechanisms need to be further elucidated.

Objectives Recent studies regarding the relationships between plasma amyloid-β (Aβ) levels and cognitive performance had inconsistent results. In this study, we aimed to characterize the relationship between cognitive decline and plasma Aβ levels in a large-sample cognitively normal population. Methods This population-based, prospective cohort study included 1,240 participants with normal cognition. The Mini-Mental State Examination (MMSE) was used to assess cognitive function at baseline and 2 years later. Restricted cubic splines, multivariate logistic regression, and multivariate linear regression models were used to evaluate the type of relationship between cognitive decline during the 2-year follow-up period and plasma Aβ levels (Aβ40, Aβ42, and Aβ42 / 40). Results Participants with moderate Aβ40 levels had the highest risk of cognitive decline during a 2-year follow-up relative to individuals with low Aβ40 [odds ratio (OR): 0.60, 95% confidence interval (CI): 0.45-0.81, p 65 years) and Aβ40 (p for interaction = 0.021). In individuals older than 65 years, there was a positive linear relationship between plasma Aβ40 and cognitive decline (OR: 1.02, 95% CI: 1.00-1.04, p = 0.027). For participants ≤ 65 years old, the lower Aβ40 and higher Aβ40 groups had a lower risk of cognitive decline than the medium Aβ40 group (OR: 0.69, 95% CI: 0.50-0.94, p = 0.02; OR: 0.63, 95% CI: 0.45-0.86, p = 0.004). None of relationship between plasma Aβ42, Aβ42 / 40 and cognitive decline was found during a 2-year follow-up. Conclusion The relationship between plasma Aβ40 and cognitive decline was not linear, but an inverted-U shape in a cognitively normal population. The underlying mechanism requires further investigation.

Objective: Growing evidence suggests that sleep disturbance is a risk factor for Alzheimer's disease (AD). Amyloid-β (Aβ) deposition in the brain is a main pathophysiology of AD. Considering that peripheral Aβ level is associated with brain Aβ deposition, the present study investigated the relationship between sleep disturbance and plasma Aβ levels.Methods: This is a population-based cross-sectional study. A total of 1,459 participants from a village in the suburbs of Xi'an, China, were enrolled from January 3, 2017 to March 26, 2017. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), and a PSQI score of 10 points as poor sleep quality. Cognitive function was assessed with the Mini-Mental State Examination (MMSE). Fasting venous blood was taken in the morning, and the plasma Aβ levels were measured using ELISA. The relationships between plasma Aβ levels and sleep quality were analyzed using multiple linear regression.Results: Among the participants, 231 had poor sleep quality (15.83%). The log-transformed Aβ40 level had significant differences among the different sleep groups (F = 3.216, p = 0.040). The log-transformed Aβ40 level was higher in the poor sleep quality group than that in the general sleep quality group [87.17 (73.42, 107.34) vs. 89.69 (74.81, 125.79) pg/ml, p = 0.016]. In bivariate analysis, sleep quality was negatively associated with the log-transformed plasma Aβ40 level (β = −0.025, p = 0.011).Conclusion: In the community population, poorer sleep quality is associated with a higher plasma Aβ40 level. This indicated that sleep disturbance might also involve in dysfunction of peripheral Aβ clearance.

Background: Sleep is an important physiological process and conducive to the elimination of brain metabolites and the recovery of brain function. However, the relationship between sleep disturbance and cognitive impairment is not fully been determined.Methods: This was a community population-based cross-sectional study. A total of 1,461 participants from a village in the suburbs of Xi’an, China were enrolled from January 3 to March 26, 2017. Sleep quality was evaluated using the Pittsburgh sleep quality index (PSQI), and sleep disturbance was defined as a PSQI score >5. Mini-mental state examination (MMSE) was used to assess cognitive function and cognitive impairment was defined as the MMSE score less than cutoff values and meets the diagnostic criteria. Univariate and multivariate analyses were used to analyze the relationships between sleep disturbance and cognitive impairment.Results: Among 1,461 subjects, 87(5.95%) had cognitive impairment, and 842 (57.63%) had sleep disturbance. In bivariate analysis, cognitive impairment was associated with insomnia (ρ=1.000, P＜0.001), age (ρ=0.172, P＜0.001) and educational level (ρ=-0.160, P＜0.001). In the binary logistic regression, cognitive impairment was positively associated with the sleep disturbance (OR=1.779, 95%CI=1.055-3.001, P=0.031). In the internal constitution of PSQI, cognitive impairment was positively associated with the sleep interference (OR=1.678; 95%CI=1.029-2.736, P=0.038), and negatively associated with the habitual sleep efficiency (OR=0.115, 95%CI=0.043-0.306, PP=0.001). Conclusions: Sleep disturbance is associated with cognitive impairment. However, the causal relationships between sleep disturbances and cognitive impairment are not clear. It needs to be further studied.

Objectives: Till now, the effect of serum lipid levels on cognitive function is still controversial. The apolipoprotein E (APOE) ε4 allele is the most critical genetic risk factor for Alzheimer’s disease (AD) and cognitive impairment. Additionally, APOE ε4 allele has a major impact on lipid metabolism. The aim of this study was to investigate the APOE genotype-dependent relationship between peripheral serum lipid levels and cognitive impairment. Methods: A total of 1,273 subjects aged 40–86 years participated in this cross-sectional study. Serum lipid levels and the APOE genotype were detected. Mini-Mental State Examination was used to diagnose the cognitive impairment or not. Univariate and multivariate analyses were used to analyze the relationships between APOE genotype, serum lipid levels, and cognition function. Results: After controlling for all possible covariates, a significant interaction between low serum high-density lipoprotein and the APOE ε4 allele on cognitive impairment (Wald’s χ2 = 4.269, df = 1, OR = 20.094, p = 0.039) was found in the total participants. In APOE ε4 carriers, low serum high-density lipoprotein was positively associated with cognitive impairment (Wald’s χ2 = 8.200, df = 1, OR = 60.335, p = 0.004) and serum high-density lipoprotein levels were positively correlated with Mini-Mental State Examination score (r = 0.217, df = 176, p = 0.004). There was no significant correlation between serum total cholesterol (TC), low-density lipoprotein, triglycerides (TG) levels, and cognitive impairment in either the total participants or APOE ε4 carriers/non-carriers. Conclusions: APOE ε4 carriers, but not non-carriers, with lower serum high-density lipoprotein had a higher prevalence of cognitive impairment and a lower Mini-Mental State Examination score. These results suggest that the APOE ε4 allele may affect the relationship between serum lipid levels and cognitive impairment. However, the specific mechanism needs to be further elucidated.

Background It is believed that deposition of amyloid beta (Aβ) in the brain is the central pathological changes of Alzheimer’s disease (AD), which triggers a series of pathological processes. However, the relationship between dyslipidemia and AD is uncertain. Considering the peripheral Aβ levels are related to brain Aβ deposition, we explore the relationships between blood lipids and plasma Aβ. Methods Participants who lived in the selected village of Xi’an for more than 3 years were enrolled, aged 40–85 years (n = 1282, 37.9% male). Fasting blood lipid, plasma Aβ levels, basic information and living habits were measured. Multiple linear regressions were used. Results In total population, blood lipids were not associated with plasma Aβ. After stratified by blood pressure, serum total cholesterol (TC) and low-density lipoprotein (LDL-c) were positively associated with plasma Aβ42 levels (βTC = 0.666, PTC = 0.024; βLDL-c = 0.743, PLDL-c = 0.011, respectively) in normal blood pressure. LDL-c was negatively associated with plasma Aβ40 levels (β = − 0.986, P = 0.037) in high blood pressure. Conclusion Elevated plasma Aβ42 levels are associated with higher TC and LDL-c in normal blood pressure. Elevated plasma Aβ40 levels are associated with lower LDL-c in high blood pressure. This indicated that the relationships between blood lipids and plasma Aβ were confounded by blood pressure.

Aims Type 2 diabetes and obesity, which are frequently comorbid, have been associated with cognitive impairment. We aim to examine the potential modulating effect between obesity and diabetes on cognitive impairment. Methods We recruited 865 adults (aged ≥55years) lived in a village of Xi'an in China from October 2014 to March 2015. All participants underwent biomedical and neuropsychological assessment. Relations of diabetes and abdominal obesity to cognitive impairment were examined in multiple regression models. Results A total of 155 participants (17.9%) presented with the diagnosis of cognitive impairment. Diabetes or obesity alone wasn't significantly associated with cognitive impairment. Interaction analysis showed a significant interaction between abdominal obesity and diabetes on cognitive impairment. Stratified multivariate analysis revealed that the association between diabetes and cognitive impairment was positive in participants with abdominal obesity (OR 2.436, 95% CI 1.345–4.411, p=0.003, in diabetics with high WC, and OR 2.348, 95% CI 1.373–4.014, p=0.002, in diabetics with high WHR), but negative in those without abdominal obesity. Conclusions Type 2 diabetes interacts with abdominal obesity to be associated with an increased risk of cognitive impairment by more than two times.

Resumen Antecedentes El consumo de tabaco es un factor de riesgo modificable para el deterioro cognitivo, no entendiendose plenamente la relacion entre dichas situaciones. El objetivo de este trabajo fue identificar la posible asociacion entre el consumo actual de tabaco y el deterioro cognitivo, dependiendo de la edad, en la poblacion rural de China. Metodos El estudio incluyo a 1.782 participantes (de 40 anos de edad o mas) que vivian en un pueblo rural de las cercanias de Xi’an (China). Se recogieron datos acerca del historial de consumo de tabaco y la funcion cognitiva. La funcion cognitiva se puntuo mediante la escala Mini-Mental State Examination. El efecto de la edad en la relacion entre el consumo de tabaco actual y el deterioro cognitivo se analizo mediante analisis de interaccion y estratificacion, utilizando modelos de regresion logistica. Resultados El analisis de interaccion reflejo que el consumo de tabaco actual guarda una relacion positiva con el deterioro cognitivo (odds ratio [OR] = 9,067; intervalo de confianza del 95% [IC 95%] 1,3056-2,979; p = 0,026). Sin embargo, el plazo de interaccion y la edad del tabaquismo actual guardan una relacion negativa con el deterioro cognitivo (OR = 0,969; IC 95% 0,939-0,999; p = 0,045). La regresion logistica estratificada reflejo que en el subestrato de 40 a 65 anos, la OR del tabaquismo actual es de 1,966 (p = 0,044), mientras que en el subestrato > 65 anos, la OR es de 0,470 (p = 0,130). Esto significa que la asociacion entre el tabaquismo actual y el deterioro cognitivo con la edad podria ser positiva (OR > 1) en los subestratos de menor edad, aunque no existe una diferencia significativa en subestratos de mayor edad. Conclusiones En conclusion, el tabaquismo actual podria estar positivamente asociado al deterioro cognitivo en la edad mediana, aunque dicha relacion disminuye con el incremento de la edad.

Background Serum lipids [total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and triglyceride (TG)] are risk factors for stroke, but the relationships between serum lipids and cognitive impairment have not been verified completely. In this study, we studied the relationships between serum lipids and cognitive impairment and explored whether gender and age had effects on the relationships. Methods In this cross-sectional study, we collected serum lipids and cognitive function information from 1762 participants (aged 40–85). Univariate analysis, multivariate analysis, and both gender- and age-based stratified multivariate analysis were used. Results In the entire sample set, there was no significant correlation between serum lipid parameters (TC, LDL-C, HDL-C and TG) and cognitive impairment. In both gender- and age-based stratified multivariate analysis, high serum TC was positively associated with cognitive impairment in the elderly (> 55) male participants (OR = 4.404, 95% CI = 1.264–15.344, p = 0.02), and high serum LDL-C was positively correlated with cognitive impairment in the elderly female subjects (OR = 2.496, 95% CI = 1.057–5.896, p = 0.037), while high serum TG was negatively associated with cognitive impairment in the middle-aged (≤ 55) male participants (OR = 0.157, 95% CI = 0.051–0.484, p = 0.001). Conclusions The relationships between serum lipids and cognitive impairment are gender- and age- dependent, with high serum TC and LDL-C may be risk factors of cognitive impairment in the elderly male and female subjects respectively, while high serum TG may be protector of cognitive impairment in the middle-aged male participants.

BACKGROUND Transport proteins, soluble low-density lipoprotein receptor-related protein-1 (sLRP1), and soluble receptor of advanced glycation end products (sRAGE), play an important role in the clearance of plasma amyloid-β (Aβ). However, their relationship is not clear. OBJECTIVE The aim was to explore the relationship between plasma levels of sLRP1, sRAGE, and Aβ in a cross-sectional study. METHODS A total of 1,185 cognitively normal participants (age above 40) from a village in the suburbs of Xi'an, China were enrolled from October 8, 2014 to March 30, 2015. Plasma Aβ40, Aβ42, sLRP1, and sRAGE were tested using a commercial ELISA. Apolipoprotein E (APOE) genotyping was conducted using PCR and sequencing. The relationship between plasma levels of sLRP1, sRAGE, and Aβ was analyzed using Pearson's correlation analysis and multiple linear regression. RESULTS In the total population, Log sLRP1 and Log sRAGE were positively correlated with plasma Aβ40 (r= 0.103, p

Background Aggregation and deposition of amyloid-β (Aβ) in the brain is the main pathological change of Alzheimer's disease (AD). Decreased Aβ42 in the cerebrospinal fluid has been confirmed as a biomarker of AD; however, the relationship between plasma Aβ and cognitive impairment is currently unclear. Objective The aim was to explore the relationship between plasma Aβ and cognitive impairment in a cross-sectional study. Methods A total of 1,314 subjects (age above 40) from a village in the suburbs of Xi'an, China were enrolled between October 8, 2014 and March 30, 2015. A validated Chinese version of the Mini-Mental State Examination and neuropsychological battery were used to assess cognition. Levels of plasma Aβ42 and Aβ40 were tested using commercial enzyme-linked immunosorbent assay. Relationship of plasma Aβ and cognitive impairment was analyzed using logistic regression analysis. Results Of the enrolled subjects, 1,180 (89.80%) had normal cognition, 85 (6.47%) had possible cognitive impairment and 49 (3.73%) had probable cognitive impairment. Logistic regression analysis showed that the Aβ42/Aβ40 ratio (OR = 4.042, 95% CI: 1.248-11.098, p = 0.012) and plasma Aβ42 (OR = 1.036, 95% CI: 1.003-1.071, p = 0.031) was higher in the possible cognitive impairment than that in the normal cognition group. Furthermore, the plasma Aβ42/Aβ40 ratio was higher in the possible cognitive impairment group than that in the probable cognitive impairment group (OR = 0.029, 95% CI: 0.002-0.450, p = 0.011). Conclusions Levels of plasma Aβ42 and Aβ42/Aβ40 ratio were elevated in patients with possible cognitive impairment, indicating that plasma Aβ42 and Aβ42/Aβ40 ratio increases may be more pronounced in early stage of cognitive impairment.

OBJECTIVE Increased pulse pressure (PP) has been implicated in the development and progression of Alzheimer's disease in middle-aged and elderly adults. Considering the close relationship between peripheral amyloid-β clearance and brain amyloid-β deposition, we investigated the potential association between PP and plasma amyloid-β transport function. METHODS In this cross-sectional study, a total of 1118 participants underwent a health assessment and quantification of plasma amyloid-β and amyloid-β transporter expression. Relationships between plasma levels of amyloid-β1-40, amyloid-β1-42, soluble low-density lipoprotein receptor-related protein-1 (sLRP1), soluble receptor for advanced glycation end products (sRAGE), and PP were determined using multiple linear regressions. RESULTS PP was a significant determinant of amyloid-β1-40 level (β = 0.059, P = 0.036) and log-transformed sRAGE (β = -0.002, P = 0.029) independent of age, sex, body mass index, pulse rate, mean arterial pressure, blood glucose, blood lipids, lifestyle, and medical history. Additionally, log-transformed soluble low-density lipoprotein receptor-related protein-1 and log-transformed sRAGE were positively associated with plasma amyloid-β1-40 level (β = 3.610, P

BACKGROUND Sleep is an important physiological process and beneficial in the removal of brain metabolites and functional recovery. Prior studies have shown that sleep disorders are significant risk factors for Alzheimer's disease (AD). OBJECTIVE The present study was designed to characterize the effect of short-term total sleep deprivation (TSD) on plasma amyloid-β (Aβ) concentrations. METHODS A clinical trial was conducted between March 1, 2016, and April 1, 2016. Twenty volunteers (age 27.3±3.4 years) with normal cognitive function and sleeping habits were recruited from the local population. Participants underwent 24 h of TSD. Periprocedural blood samples were collected to compare the changes of plasma Aβ42, Aβ40, low-density lipoprotein receptor-related protein (sLRP-1), soluble receptors for advanced glycation end products (sRAGE), and serum superoxide dismutase (SOD) and malonaldehyde (MDA). RESULTS TSD increased morning plasma Aβ40 levels by 32.6% (p

Background Cigarette smoking is a modifiable risk factor for cognitive impairment, while the relationship between current smoking and cognitive impairment is not fully understood. The objectives were to identify a possible association between current smoking and cognitive impairment depending on age in the Chinese rural population. Methods Data for the study consisted of 1782 participants (40 years and older) who lived in a rural village in the vicinity of Xi’an, China. Data about smoking history and cognitive function were collected. Cognitive function was scored by the Mini-Mental State Examination. The effect of age on the relationship between current smoking and cognitive impairment was analyzed with interaction and stratified analysis by logistic regression models. Results Interaction analysis showed that current smoking is positively related with cognitive impairment (odds ratio [OR] = 9.067; 95% confidence interval [95% CI] 1.305–62.979; P = 0.026). However, the interaction term, age by current smoking, is negatively related with cognitive impairment (OR = 0.969; 95%CI 0.939–0.999; P = 0.045). Stratified logistic regression showed that in the 40–65 years of age sublayer, OR of current smoking is 1.966 (P = 0.044), whereas in the >65 years of age sublayer, the OR is 0.470 (P = 0.130). This means that the association between current smoking and cognitive impairment with age might be positive (OR > 1) in lower age sublayers, but no significant difference in higher age sublayers. Conclusions In conclusion, current smoking might be positively associated with cognitive impairment in the middle-aged but the relationship declines with increasing age.