Browsing by Author "Yashin, Anatoli I"
Now showing items 1-17 of 17
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Age, gender, and cancer but not neurodegenerative and cardiovascular diseases strongly modulate systemic effect of the Apolipoprotein E4 allele on lifespan.
(PLoS Genet, 2014-01)Enduring interest in the Apolipoprotein E (ApoE) polymorphism is ensured by its evolutionary-driven uniqueness in humans and its prominent role in geriatrics and gerontology. We use large samples of longitudinally followed ... -
Beta2-adrenergic receptor gene polymorphisms as systemic determinants of healthy aging in an evolutionary context.
(Mech Ageing Dev, 2010-05)The Gln(27)Glu polymorphism but not the Arg(16)Gly polymorphism of the beta2-adrenergic receptor (ADRB2) gene appears to be associated with a broad range of aging-associated phenotypes, including cancers at different sites, ... -
Circulatory Diseases in the U.S. Elderly in the Linked National Long-Term Care Survey-Medicare Database: Population-Based Analysis of Incidence, Comorbidity, and Disability.
(Res Aging, 2013-07)Incidence rates of acute coronary heart disease (ACHD; including myocardial infarction and angina pectoris), stroke, and heart failure (HF) were studied for their age, disability, and comorbidity patterns in the U.S. elderly ... -
Coordinated Action of Biological Processes during Embryogenesis Can Cause Genome-Wide Linkage Disequilibrium in the Human Genome and Influence Age-Related Phenotypes.
(Ann Gerontol Geriatr Res, 2016)A role of non-Mendelian inheritance in genetics of complex, age-related traits is becoming increasingly recognized. Recently, we reported on two inheritable clusters of SNPs in extensive genome-wide linkage disequilibrium ... -
Do gender, disability, and morbidity affect aging rate in the LLFS? Application of indices of cumulative deficits.
(Mech Ageing Dev, 2011-04)We used an approach of cumulative deficits to evaluate the rate of aging in 4954 participants of the Long-Life Family Study (LLFS) recruited in the U.S. (Boston, New York, and Pittsburgh) and Denmark. We used an array of ... -
Health and function of participants in the Long Life Family Study: A comparison with other cohorts.
(Aging (Albany NY), 2011-01)Individuals from families recruited for the Long Life Family Study (LLFS) (n= 4559) were examined and compared to individuals from other cohorts to determine whether the recruitment targeting longevity resulted in a cohort ... -
Heritability estimates of endophenotypes of long and health life: the Long Life Family Study.
(J Gerontol A Biol Sci Med Sci, 2010-12)BACKGROUND: Identification of gene variants that contribute to exceptional survival may provide critical biologic information that informs optimal health across the life span. METHODS: As part of phenotype development efforts ... -
Inter-chromosomal level of genome organization and longevity-related phenotypes in humans.
(Age (Dordr), 2013-04)Studies focusing on unraveling the genetic origin of health span in humans assume that polygenic, aging-related phenotypes are inherited through Mendelian mechanisms of inheritance of individual genes. We use the Framingham ... -
Letter to the editor: Standardization of genetic association studies, pros and cons, reaffirmed.
(Age (Dordr), 2014-04) -
Leukocyte telomere length is associated with disability in older u.s. Population.
(J Am Geriatr Soc, 2010-07)OBJECTIVES: To determine whether mean leukocyte telomere length (LTL) serves as a biomarker of disability assessed according to activities of daily living (ADLs) and what factors may modify this relationship. DESIGN: ... -
Polymorphisms in the ACE and ADRB2 genes and risks of aging-associated phenotypes: the case of myocardial infarction.
(Rejuvenation Res, 2010-02)Multiple functions of the beta2-adrenergic receptor (ADRB2) and angiotensin-converting enzyme (ACE) genes warrant studies of their associations with aging-related phenotypes. We focus on multimarker analyses and analyses ... -
Quantification of biological aging in young adults.
(Proc Natl Acad Sci U S A, 2015-07-28)Antiaging therapies show promise in model organism research. Translation to humans is needed to address the challenges of an aging global population. Interventions to slow human aging will need to be applied to still-young ... -
The role of lipid-related genes, aging-related processes, and environment in healthspan
(Aging Cell, 2013)The inherent complexity of aging-related traits can temper progress in unraveling the genetic origins of healthspan. We focus on two generations in the Framingham Heart Study, the original (FHS) and offspring (FHSO) cohorts, ... -
Trade-off in the effect of the APOE gene on the ages at onset of cardiocascular disease and cancer across ages, gender, and human generations.
(Rejuvenation Res, 2013-02)Decades of studies of candidate genes show their complex role in aging-related traits. We focus on apolipoprotein E e2/3/4 polymorphism and ages at onset of cardiovascular diseases (CVD) and cancer in the parental and offspring ... -
Trade-off in the effects of the apolipoprotein E polymorphism on the ages at onset of CVD and cancer influences human lifespan.
(Aging Cell, 2011-06)Progress in unraveling the genetic origins of healthy aging is tempered, in part, by a lack of replication of effects, which is often considered a signature of false-positive findings. We convincingly demonstrate that the ... -
Trade-offs between cancer and other diseases: do they exist and influence longevity?
(Rejuvenation Res, 2010-08)Relationships between aging, disease risks, and longevity are not yet well understood. For example, joint increases in cancer risk and total survival observed in many human populations and some experimental aging studies ... -
Trade-offs in the effects of the apolipoprotein E polymorphism on risks of diseases of the heart, cancer, and neurodegenerative disorders: insights on mechanisms from the Long Life Family Study.
(Rejuvenation Res, 2015-04)The lack of evolutionary established mechanisms linking genes to age-related traits makes the problem of genetic susceptibility to health span inherently complex. One complicating factor is genetic trade-off. Here we focused ...
