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650 results on '"Arbeev, Konstantin"'

2. Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota

Author

Ji, Ming, Xu, Xiaojiang, Xu, Qing, Hsiao, Yun-Chung, Martin, Cody, Ukraintseva, Svetlana, Popov, Vladimir, Arbeev, Konstantin G., Randall, Tom A., Wu, Xiaoyue, Garcia-Peterson, Liz M., Liu, Juan, Xu, Xin, Andrea Azcarate-Peril, M., Wan, Yisong, Yashin, Anatoliy I., Anantharaman, Karthik, Lu, Kun, Li, Jian-Liang, Shats, Igor, and Li, Xiaoling

Published
2023
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8. Genome-Wide Epistatic Network Analyses of Semantic Fluency in Older Adults

Author

Tan, Qihua, primary, Li, Weilong, additional, Nygaard, Marianne, additional, An, Ping, additional, Feitosa, Mary, additional, Wojczynski, Mary K., additional, Zmuda, Joseph, additional, Arbeev, Konstantin, additional, Ukraintseva, Svetlana, additional, Yashin, Anatoliy, additional, Christensen, Kaare, additional, and Mengel-From, Jonas, additional

Published
2024
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10. The association between rs6859 in NECTIN2 gene and Alzheimer's disease is partly mediated by pTau.

Author

Rajendrakumar, Aravind Lathika, Arbeev, Konstantin G., Bagley, Olivia, Yashin, Anatoliy I., and Ukraintseva, Svetlana

Subjects
ALZHEIMER'S disease risk factors, GENETICS of Alzheimer's disease, ALZHEIMER'S disease, DESCRIPTIVE statistics, NERVE tissue proteins, FACTOR analysis, NEURORADIOLOGY, CONFIDENCE intervals, GENOTYPES, SINGLE nucleotide polymorphisms, CEREBROSPINAL fluid, ALLELES, REGRESSION analysis
Abstract

Introduction: Emerging evidence suggests a connection between vulnerability to infections and Alzheimer's disease (AD). The nectin cell adhesion molecule 2 (NECTIN2) gene coding for a membrane component of adherens junctions is involved in response to infections, and its single nucleotide polymorphism (SNP) rs6859 was significantly associated with AD risk in several human cohorts. It is unclear, however, how exactly rs6859 influences the development of AD pathology. The aggregation of hyperphosphorylated tau protein (pTau) is a key pathological feature of neurodegeneration in AD, which may be induced by infections, among other factors, and potentially influenced by genes involved in both AD and vulnerability to infections, such as NECTIN2. Materials and methods: We conducted a causal mediation analysis (CMA) on a sample of 708 participants in the Alzheimer's disease Neuroimaging Initiative (ADNI). The relationship between rs6859 and Alzheimer's disease (AD), with AD (yes/no) as the outcome and pTau-181 levels in the cerebrospinal fluid (CSF) acting as a mediator in this association, was assessed. Adjusted estimates from the probit and linear regression models were used in the CMA model, where an additive model considered an increase in dosage of the rs6859 A allele (AD risk factor). Results: The increase in dose of allele A of the SNP rs6859 resulted in about 0.144 increase per standard deviation (SD) of pTau-181 (95% CI: 0.041, 0.248, p < 0.01). When included together in the probit model, the change in A allele dose and each standard deviation change in pTau-181 predicted 6.84% and 9.79% higher probabilities for AD, respectively. In the CMA, the proportion of the average mediated effect was 17.05% and was higher for the risk allele homozygotes (AA), at 19.40% (95% CI: 6.20%, 43.00%, p < 0.01). The sensitivity analysis confirmed the evidence of a robust mediation effect. Conclusion: This study reported a new potential causal relationship between pTau-181 and AD. We found that the association between rs6859 in the NECTIN2 gene and AD is partly mediated by pTau-181 levels in CSF. The rest of this association may be mediated by other factors. Our finding sheds light on the complex interplay between genetic susceptibility, protein aggregation, and neurodegeneration in AD. Further research, using other biomarkers, is needed to uncover the remaining mechanisms of the association between the NECTIN2 gene and AD. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Multidimensional Stochastic Process Model and its Applications to Analysis of Longitudinal Data with Genetic Information

Author

Zhbannikov, Ilya, Arbeev, Konstantin, and Yashin, Anatoliy

Subjects
Quantitative Biology - Populations and Evolution
Abstract

Stochastic Process Model has many applications in analysis of longitudinal biodemographic data. Such data contain various physiological variables (sometimes known as covariates). It also can potentially contain genetic information available for all or a part of participants. Taking advantage from both genetic and non-genetic information can provide future insights into a broad range of processes describing aging-related changes in the organism. In this paper, we implemented a multi-dimensional Genetic Stochastic Process Model (GenSPM) in newly developed software tool, R-package stpm, which allows researchers performing such kind of analysis.

Published
2016

18. Patterns of Aging Changes in Bodyweight May Predict Alzheimer’s Disease

Author

Ukraintseva, Svetlana, primary, Duan, Hongzhe, additional, Holmes, Rachel, additional, Bagley, Olivia, additional, Wu, Deqing, additional, Yashkin, Arseniy, additional, Kulminski, Alexander, additional, Akushevich, Igor, additional, Whitson, Heather, additional, Stallard, Eric, additional, Yashin, Anatoliy, additional, and Arbeev, Konstantin, additional

Published
2024
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28. Vaccination Against Pneumonia May Provide Genotype-Specific Protection Against Alzheimer’s Disease

Author

Ukraintseva, Svetlana, primary, Duan, Matt, additional, Simanek, Amanda M., additional, Holmes, Rachel, additional, Bagley, Olivia, additional, Rajendrakumar, Aravind L., additional, Yashkin, Arseniy P., additional, Akushevich, Igor, additional, Tropsha, Alexander, additional, Whitson, Heather, additional, Yashin, Anatoliy, additional, and Arbeev, Konstantin, additional

Published
2023
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30. Interactions between genes involved in physiological dysregulation and axon guidance: role in Alzheimer’s disease

Author

Arbeev, Konstantin G., primary, Ukraintseva, Svetlana, additional, Bagley, Olivia, additional, Duan, Hongzhe, additional, Wu, Deqing, additional, Akushevich, Igor, additional, Stallard, Eric, additional, Kulminski, Alexander, additional, Christensen, Kaare, additional, Feitosa, Mary F., additional, O’Connell, Jeffrey R., additional, Parker, Daniel, additional, Whitson, Heather, additional, and Yashin, Anatoliy I., additional

Published
2023
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38. Stochastic Process Models of Mortality and Aging

Author

Yashin, Anatoliy I., Arbeev, Konstantin G., Arbeeva, Liubov S., Akushevich, Igor, Ukraintseva, Svetlana V., Kulminski, Alexander M., Stallard, Eric, Land, Kenneth C., Land, Kenneth C., Series editor, Yashin, Anatoliy I., and Stallard, Eric

Published
2016
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44. Evidence for Dependence Among Diseases

Author

Yashin, Anatoliy I., Ukraintseva, Svetlana V., Akushevich, Igor, Kulminski, Alexander M., Arbeev, Konstantin G., Stallard, Eric, Land, Kenneth C., Series editor, Yashin, Anatoliy I., and Stallard, Eric

Published
2016
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46. The Protective Effect of Familial Longevity Persists After Age 100: Findings From the Danish National Registers.

Author

Galvin, Angéline, Pedersen, Jacob Krabbe, Wojczynski, Mary K, Ukraintseva, Svetlana, Arbeev, Konstantin, Feitosa, Mary, Province, Michael A, and Christensen, Kaare

Subjects
PROPORTIONAL hazards models, LONGEVITY
Abstract

Background A recent study suggested that the protective effect of familial longevity becomes negligible for centenarians. However, the authors assessed the dependence on familial longevity in centenarians by comparing centenarians with 1 parent surviving to age 80+ to centenarians whose same-sexed parent did not survive to age 80. Here we test whether the protective effect of familial longevity persists after age 100 using more restrictive definitions of long-lived families. Methods Long-lived sibships were identified through 3 nationwide, consecutive studies in Denmark, including families with either at least 2 siblings aged 90+ or a Family Longevity Selection Score (FLoSS) above 7. Long-lived siblings enrolled in these studies and who reached age 100 were included. For each sibling, 5 controls matched on sex and year of birth were randomly selected among centenarians in the Danish population. Survival time from age 100 was described with Kaplan–Meier curves for siblings and controls separately. Survival analyses were performed using stratified Cox proportional hazards models. Results A total of 340 individuals from long-lived sibships who survived to age 100 and 1 700 controls were included. Among the long-lived siblings and controls, 1 650 (81%) were women. The results showed that long-lived siblings presented better overall survival after age 100 than sporadic long-livers (hazard ratio [HR]  = 0.80, 95% confidence interval [CI]  = 0.71–0.91), with even lower estimate (HR = 0.65, 95% CI = 0.50–0.85) if familial longevity was defined by FLoSS. Conclusions The present study, with virtually no loss to follow-up, demonstrated a persistence of protective effect of familial longevity after age 100. [ABSTRACT FROM AUTHOR]

Published
2024
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