Do Cardiometabolic Risk Factors Influence Amyloid, Tau, and Neuronal Function in APOE4 Carriers and Non-Carriers in Alzheimer’s Disease Trajectory?

2018 ◽  
Vol 64 (3) ◽  
pp. 981-993 ◽  
Author(s):  
Grazia Daniela Femminella ◽  
Genevieve Taylor-Davies ◽  
James Scott ◽  
Paul Edison ◽  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cardiometabolic Risk ◽  
Cardiometabolic Risk Factors ◽  
Neuronal Function ◽  
Disease Trajectory

scholarly journals Cardiometabolic risk factors predict executive function scores in high-risk individuals

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 651-651
Author(s):  
Joshua Gills ◽  
Megan Jones ◽  
Anthony Campitelli ◽  
Sally Paulson ◽  
Erica Madero ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Blood Pressure ◽  
Alzheimer's Disease ◽  
Executive Function ◽  
High Risk ◽  
Cardiometabolic Risk ◽  
Density Lipoprotein ◽  
Cardiometabolic Risk Factors ◽  
Walking Test

Abstract Alzheimer’s disease (AD) is expected to triple by 2050, affecting 16 million Americans. As a result, it is essential to combat this alarming increase in cognitive impairment through early detection. Cardiometabolic risk factors have shown to be associated with higher risk of AD. The purpose of this study was to determine if cardiometabolic risk factors could predict executive function scores in a high-risk population. Fifty (60.9±8.8 years) high-risk adults (classified by the Australian National University Alzheimer’s Disease Risk Index) were enrolled in this study. Participants completed a 6-minute walking test, venous blood draw, blood pressure measurement, and the digit coding symbol test (DCS). Results were examined through a multiple linear regression with DCS as the dependent variable and age, sex, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), glucose, 6-minute walking test, systolic blood pressure (SBP), and diastolic blood pressure (DBP) as predictor variables. The model explained 42% of the variance of DCS (p = .04) with SBP (45%; p = .003) as a significant predictor. LDL (p = .087) and DBP (p = .123) accounted for 24% and 22% of the variance for this model, respectively. These results suggest cardiometabolic risk factors predict executive function values in high-risk individuals. Higher SBP was significantly associated with lower DCS scores indicating SBP as a valuable tool for practitioners when evaluating cognitive decline. Further research should expand sample size and track values longitudinally to substantiate these claims.

scholarly journals Polygenic risk score for Alzheimer’s disease and trajectories of cardiometabolic risk factors in children

2019 ◽  
Author(s):  
Roxanna S Korologou-Linden ◽  
Linda O’Keeffe ◽  
Laura D Howe ◽  
George Davey Smith ◽  
Hannah Jones ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Variants ◽  
Cardiometabolic Risk ◽  
Cardiometabolic Risk Factors ◽  
Childhood And Adolescence ◽  
Polygenic Risk Score ◽  
Polygenic Risk ◽  
Cardiometabolic Factors

AbstractINTRODUCTIONCardiometabolic factors are implicated in the aetiology of Alzheimer’s disease and may lie on the pathways linking genetic variants to Alzheimer’s disease across the life course. We examined whether polygenic risk scores (PRS) were associated with cardiometabolic health indicators through childhood and adolescence.METHODSIn 7,977 participants from the Avon Longitudinal Study of Parents and Children, we tested whether a PRS for Alzheimer’s disease was associated with trajectories of cardiometabolic risk factors. We examined trajectories for height 1-18 years; lean and fat mass 9-18 years; systolic and diastolic blood pressure 7-18 years; glucose and C-reactive protein 9-18 years; insulin 10-18 years; high and low-density lipoproteins and triglycerides birth-18 years. We also examined birthweight, interleukin-6 (IL-6) at age 9 years and physical activity at ages 11, 12, and 15 years.RESULTSNo consistent associations were observed between the PRS excluding genetic variants in the apolipoprotein E (ApoE) gene region and cardiometabolic factors trajectories across childhood and adolescence.CONCLUSIONWe did not detect evidence to suggest that the PRS for Alzheimer’s disease acts through childhood and adolescent cardiometabolic risk factors. Further studies should examine whether these associations emerge later in adulthood when variation in cardiometabolic risk factors is likely to be greater.

scholarly journals Polygenic risk score for Alzheimer’s disease and trajectories of cardiometabolic risk factors in children

2019 ◽  
Vol 4 ◽  
pp. 125 ◽  
Author(s):  
Roxanna Korologou-Linden ◽  
Linda O'Keeffe ◽  
Laura D. Howe ◽  
George Davey-Smith ◽  
Hannah J. Jones ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Variants ◽  
Cardiometabolic Risk ◽  
Cardiometabolic Risk Factors ◽  
Childhood And Adolescence ◽  
Polygenic Risk Score ◽  
Polygenic Risk ◽  
Cardiometabolic Factors

Introduction: Cardiometabolic factors are implicated in the aetiology of Alzheimer’s disease and may lie on the pathways linking genetic variants to Alzheimer’s disease across the life course. We examined whether polygenic risk scores (PRS) were associated with cardiometabolic health indicators through childhood and adolescence. Methods: In 7,977 participants from the Avon Longitudinal Study of Parents and Children, we tested whether a PRS for Alzheimer’s disease was associated with trajectories of cardiometabolic risk factors. We examined trajectories for height at 1-18 years; lean and fat mass at 9-18 years; systolic and diastolic blood pressure at 7-18 years; glucose and C-reactive protein at 9-18 years; insulin at 10-18 years; and high and low-density lipoproteins and triglycerides birth at 18 years. We also examined birthweight and interleukin-6 (IL-6) at age 9 years and physical activity at ages 11, 12, and 15 years. Results: No consistent associations were observed between the PRS excluding genetic variants in the apolipoprotein E gene region and cardiometabolic factors trajectories across childhood and adolescence. Conclusions: We did not detect evidence to suggest that the PRS for Alzheimer’s disease acts through childhood and adolescent cardiometabolic risk factors. Further studies should examine whether these associations emerge later in adulthood when variation in cardiometabolic risk factors is likely to be greater.

CARDIOMETABOLIC RISK PREDICTS BIOMARKER PROGRESSION IN ALZHEIMER’S DISEASE TRAJECTORY

2017 ◽  
Vol 13 (7) ◽  
pp. P1227
Author(s):  
Grazia Daniela Femminella ◽  
Genevieve Taylor-Davies ◽  
James Scott ◽  
Paul Edison
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cardiometabolic Risk ◽  
Disease Trajectory

scholarly journals Derailed Intraneuronal Signalling Drives Pathogenesis in Sporadic and Familial Alzheimer’s Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Tom Van Dooren ◽  
Katrien Princen ◽  
Koen De Witte ◽  
Gerard Griffioen
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Degeneration ◽  
Feedback Mechanism ◽  
Membrane Receptors ◽  
Neuronal Function ◽  
Systematic Analysis ◽  
Positive Feedback Mechanism ◽  
Or Genes

Although a wide variety of genetic and nongenetic Alzheimer’s disease (AD) risk factors have been identified, their role in onset and/or progression of neuronal degeneration remains elusive. Systematic analysis of AD risk factors revealed that perturbations of intraneuronal signalling pathways comprise a common mechanistic denominator in both familial and sporadic AD and that such alterations lead to increases in Aβoligomers (Aβo) formation and phosphorylation of TAU. Conversely, Aβo and TAU impact intracellular signalling directly. This feature entails binding of Aβo to membrane receptors, whereas TAU functionally interacts with downstream transducers. Accordingly, we postulate a positive feedback mechanism in which AD risk factors or genes trigger perturbations of intraneuronal signalling leading to enhanced Aβo formation and TAU phosphorylation which in turn further derange signalling. Ultimately intraneuronal signalling becomes deregulated to the extent that neuronal function and survival cannot be sustained, whereas the resulting elevated levels of amyloidogenic Aβo and phosphorylated TAU species self-polymerizes into the AD plaques and tangles, respectively.

Increased monocyte to HDL cholesterol ratio in vitamin B12 deficiency: is it related to cardiometabolic risk?

2020 ◽  
pp. 1-8
Author(s):  
Sanem Kayhan ◽  
Nazli Gulsoy Kirnap ◽  
Mercan Tastemur
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Uric Acid ◽  
Vitamin B12 ◽  
Cardiometabolic Risk ◽  
Vitamin B12 Deficiency ◽  
Left Ventricular ◽  
Cardiometabolic Risk Factors ◽  
B12 Deficiency ◽  
Deficiency Group

Abstract. Vitamin B12 deficiency may have indirect cardiovascular effects in addition to hematological and neuropsychiatric symptoms. It was shown that the monocyte count-to-high density lipoprotein cholesterol (HDL-C) ratio (MHR) is a novel cardiovascular marker. In this study, the aim was to evaluate whether MHR was high in patients with vitamin B12 deficiency and its relationship with cardiometabolic risk factors. The study included 128 patients diagnosed with vitamin B12 deficiency and 93 healthy controls. Patients with vitamin B12 deficiency had significantly higher systolic blood pressure (SBP), diastolic blood pressure (DBP), MHR, C-reactive protein (CRP) and uric acid levels compared with the controls (median 139 vs 115 mmHg, p < 0.001; 80 vs 70 mmHg, p < 0.001; 14.2 vs 9.5, p < 0.001; 10.2 vs 4 mg/dl p < 0.001; 6.68 vs 4.8 mg/dl, p < 0.001 respectively). The prevalence of left ventricular hypertrophy was higher in vitamin B12 deficiency group (43.8%) than the control group (8.6%) (p < 0.001). In vitamin B12 deficiency group, a positive correlation was detected between MHR and SBP, CRP and uric acid (p < 0.001 r:0.34, p < 0.001 r:0.30, p < 0.001 r:0.5, respectively) and a significant negative correlation was detected between MHR and T-CHOL, LDL, HDL and B12 (p < 0.001 r: −0.39, p < 0.001 r: −0.34, p < 0.001 r: −0.57, p < 0.04 r: −0.17, respectively). MHR was high in vitamin B12 deficiency group, and correlated with the cardiometabolic risk factors in this group, which were SBP, CRP, uric acid and HDL. In conclusion, MRH, which can be easily calculated in clinical practice, can be a useful marker to assess cardiovascular risk in patients with vitamin B12 deficiency.

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