Summary and Assessment of Studies on Cardiac Aging in Nonhuman Primates

2021 ◽  
Author(s):  
Hillary F Huber ◽  
Peter W Nathanielsz ◽  
Geoffrey D Clarke
Keyword(s):  
Life Course ◽  
Early Life ◽  
Nonhuman Primates ◽  
Disease Risk ◽  
Future Research ◽  
Cardiac Aging ◽  
Related Disease ◽  
Biomarkers Of Aging ◽  
Age Related ◽  
Wide Range

Nonhuman primates (NHP) are important translational models for cardiac aging. To assess progress in this research area and to provide a reference for other investigators, we identified papers indexed in PubMed to determine what species, ages, outcomes, treatments, and approaches have been studied. Since 1983, 33 studies of cardiac aging in NHP have been published.Of these, 27 used species of macaque, 6 baboon, 1 vervet, 1 orangutan, and 1 marmoset (some studies were multispecies).Common research approaches were echocardiography, ECG, and histology of the left ventricle. Only 10 studies performedsex-based analyses. The average age of the oldest macaque studied was 26 y. The reported mean lifespan of macaques incaptivity is around 30 y. The age of the oldest baboon studied was 24 y. Baboons in captivity are reported to live on averageto 21 y. Twelve studies took a “life course” approach, studying animals of a wide range of ages from less than or equal to 10y through the late teens to thirties, and employing analyses designed to show change over time. Keeping NHP into old ageis a major challenge for biomedical research. The ideal design is to start monitoring in early life and to track how cardiacstructure and function change with age. Important issues for future research are an increased focus on life-course approaches, investment in existing life-course NHP cohorts, better reporting of study sample characteristics, more molecular studies to identify genetic risk factors and mechanisms, attention to sex as a biological variable, a move away from descriptive reports to mechanistic studies, development of biomarkers to predict disease risk, and exploration of interventions that are implemented early in life to prevent or delay age-related disease later in life. Reducing exposure to early life adversity, identifying early-life biomarkers of aging and age-related disease, and early treatment can contribute to longer health span.

Calorie Restriction in Nonhuman Primates: Implications for Age-Related Disease Risk

1998 ◽  
Vol 1 (4) ◽  
pp. 315-326 ◽  
Author(s):  
MARK A. LANE ◽  
ANGELA BLACK ◽  
DONALD K. INGRAM ◽  
GEORGE S. ROTH
Keyword(s):  
Calorie Restriction ◽  
Nonhuman Primates ◽  
Disease Risk ◽  
Related Disease ◽  
Age Related

scholarly journals Physical Activity and Telomere Biology: Exploring the Link with Aging-Related Disease Prevention

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Andrew T. Ludlow ◽  
Stephen M. Roth
Keyword(s):  
Physical Activity ◽  
Physical Inactivity ◽  
Replicative Senescence ◽  
Disease Risk ◽  
Future Research ◽  
Activity Levels ◽  
Related Disease ◽  
Age Related ◽  
A Cell ◽  
Telomere Biology

Physical activity is associated with reduced risk of several age-related diseases as well as with increased longevity in both rodents and humans. Though these associations are well established, evidence of the molecular and cellular factors associated with reduced disease risk and increased longevity resulting from physical activity is sparse. A long-standing hypothesis of aging is the telomere hypothesis: as a cell divides, telomeres shorten resulting eventually in replicative senescence and an aged phenotype. Several reports have recently associated telomeres and telomere-related proteins to diseases associated with physical inactivity and aging including cardiovascular disease, insulin resistance, and hypertension. Interestingly several reports have also shown that longer telomeres are associated with higher physical activity levels, indicating a potential mechanistic link between physical activity, reduced age-related disease risk, and longevity. The primary purpose of this review is to discuss the potential importance of physical activity in telomere biology in the context of inactivity- and age-related diseases. A secondary purpose is to explore potential mechanisms and important avenues for future research in the field of telomeres and diseases associated with physical inactivity and aging.

scholarly journals METABOLIC INTEGRITY – A FACTOR IN AGING AND A PLAYER IN THE MECHANISMS OF CR

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S67-S67
Author(s):  
Rozalyn Anderson
Keyword(s):  
Metabolic Pathways ◽  
Nonhuman Primates ◽  
Disease Risk ◽  
Metabolic Dysfunction ◽  
Aging Research ◽  
Root Cause ◽  
Related Disease ◽  
Metabolic Component ◽  
Age Related ◽  
Metabolic Biomarkers

Abstract An emerging paradigm in aging research identifies metabolic dysfunction as a root cause in age-related disease vulnerability. Several diseases of aging, including diabetes, cancer, and neurodegeneration, have an established metabolic component. Our studies have focused on links between metabolic status and disease vulnerability. Caloric restriction (CR) delays aging and the onset of age-related disease in diverse species, including nonhuman primates. Molecular profiling identifies CR responsive elements in the transcriptome, proteome, and metabolome that are highly enriched for metabolic pathways and in particular mitochondrial processes. These data show that improvements in health and survival are associated with maintenance of system wide metabolic homeostasis and preserved energy metabolism among tissues. Metabolic biomarkers identified in these studies may be clinically relevant for the early identification of elevated disease risk in humans and could even be potential targets for the development of novel strategies to lower disease vulnerability as a function of age.

scholarly journals Is Early Life Adversity a Trigger towards Inflammageing?

2021 ◽  
Author(s):  
Myriam Merz ◽  
Jonathan D. Turner
Keyword(s):  
Early Life ◽  
Viral Infections ◽  
Disease Risk ◽  
Later Life ◽  
Early Life Adversity ◽  
Chronic Viral Infections ◽  
Age Related ◽  
Wide Range ◽  
Distinct Features ◽  
Near Future

There are many ‘faces’ of early life adversity (ELA), such as childhood trauma, institutionalization, abuse or exposure to environmental toxins. These have been implicated in the onset and severity of a wide range of chronic non-communicable diseases later in life. The later-life disease risk has a well-established immunological component. This raises the question as to whether accelerated immune-ageing mechanistically links early-life adversity to the lifelong health trajectory resulting in either ‘poor’ or ‘healthy’ ageing. Here we examine observational and mechanistic studies of ELA and inflammageing, highlighting common and distinct features in these two life stages. Many biological processes appear in common including reduction in telomere length, increased immuno-senescence, metabolic distortions and chronic (viral) infections. We propose that ELA shapes the developing immune, endocrine and nervous system in a non-reversible way, creating a distinct phenotype with accelerated immuno-senescence and systemic inflammation. We believe that ELA acts as an accelerator for inflammageing and age-related diseases. Furthermore, we now have the tools and cohorts to be able to dissect the interaction between early life adversity and later life phenotype. This should, in the near future, allow us to identify the ecological and mechanistic processes that are involved in ‘healthy’ or accelerated immune-ageing.

Progressive and predictive markers of disease evolution: platelet transcriptome in chronic myeloproliferative neoplasms

2021 ◽  
Author(s):  
Zhu Shen ◽  
Wenfei Du ◽  
Cecelia Perkins ◽  
Lenn Fechter ◽  
Vanita Natu ◽  
...  
Keyword(s):  
Machine Learning ◽  
Risk Stratification ◽  
Disease Risk ◽  
Myeloproliferative Neoplasms ◽  
Penalized Regression ◽  
Machine Learning Algorithms ◽  
Disease Evolution ◽  
Chronic Myeloproliferative Neoplasms ◽  
Age Related ◽  
Wide Range

Predicting disease natural history remains a particularly challenging endeavor in chronic degenerative disorders and cancer, thus limiting early detection, risk stratification, and preventive interventions. Here, profiling the spectrum of chronic myeloproliferative neoplasms (MPNs), as a model, we identify the blood platelet transcriptome as a generalizable strategy for highly sensitive progression biomarkers that also enable prediction via machine learning algorithms. Using RNA sequencing (RNA seq), we derive disease relevant gene expression and alternative splicing in purified platelets from 120 peripheral blood samples constituting two independently collected and mutually validating patient cohorts of the three MPN subtypes: essential thrombocythemia, ET (n=24), polycythemia vera, PV (n=33), and primary or post ET/PV secondary myelofibrosis, MF (n=42), as well as healthy donors (n=21). The MPN platelet transcriptome discriminates each clinical phenotype and reveals an incremental molecular reprogramming that is independent of patient driver mutation status or therapy. Leveraging this dataset, in particular the progressive expression gradient noted across MPN, we develop a machine learning model (Lasso-penalized regression) predictive of the advanced subtype MF at high accuracy (AUC-ROC of 0.95-0.96) with validation under two conditions: i) temporal, with training on the first cohort (n=71) and independent testing on the second (n=49) and ii) 10 fold cross validation on the entire dataset. Lasso-derived signatures offer a robust core set of < 10 MPN progression markers. Mechanistic insights from our data highlight impaired protein homeostasis as a prominent driver of MPN evolution, with persistent integrated stress response. We also identify JAK inhibitor-specific signatures and other interferon, proliferation, and proteostasis associated markers as putative targets for MPN-directed therapy. Our platelet transcriptome snapshot of chronic MPNs establishes a methodological foundation for deciphering disease risk stratification and progression beyond genetic data alone, thus presenting a promising avenue toward potential utility in a wide range of age-related disorders.

PHYSICAL ACTIVITY AS HEALTHY INTERVENTION AGAINST SEVERE OXIDATIVE STRESS IN ELDERLY POPULATION

2013 ◽  
pp. 1-9
Author(s):  
C. TOMAS-ZAPICO ◽  
E. IGLESIAS-GUTIERREZ ◽  
B. FERNANDEZ-GARCIA ◽  
D. DE GONZALO-CALVO
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Elderly Population ◽  
Physiological Basis ◽  
Related Disease ◽  
Age Related ◽  
Wide Range ◽  
Health Related ◽  
Relevant Risk Factor

Severe oxidative stress is a relevant risk factor for major deleterious health-related events in olderpeople and is thought to be an important contributor to age-related disease. Literature has suggested oxidativestress as a therapeutic target for mitigating the biological decline and attenuating the occurrence of adverseclinical events in aged individuals. However, definitive treatments are not known. Regular and moderate physicalactivity has been proposed as possible intervention for slowing age-related decline. This healthy strategy presentsa wide range of beneficial aspects for elderly, from the reduction of morbidity, disability, frailty and mortalityrates to treatment of many age-related disorders. Importantly, the global benefits on health are not shared by anyother strategies. Nevertheless, the physiological basis by which exercise produces its benefits to the organism isnot fully understood. This review summarizes the evidence for the role of physical activity as potential healthyintervention for mitigating the negative aspects of aging through the modulation of the oxidative mechanisms.

scholarly journals Flavonoids and age-related disease: Risk, benefits and critical windows

Maturitas ◽  
2010 ◽  
Vol 66 (2) ◽  
pp. 163-171 ◽  
Author(s):  
J.K. Prasain ◽  
S.H. Carlson ◽  
J.M. Wyss
Keyword(s):  
Disease Risk ◽  
Related Disease ◽  
Age Related

scholarly journals Psychosocial Stressors and Telomere Length: A Current Review of the Science

2020 ◽  
Vol 41 (1) ◽  
pp. 223-245 ◽  
Author(s):  
Kelly E. Rentscher ◽  
Judith E. Carroll ◽  
Colter Mitchell
Keyword(s):  
Telomere Length ◽  
Psychosocial Stress ◽  
Psychosocial Stressors ◽  
Biological Aging ◽  
Future Research ◽  
Age Related ◽  
Social Adversity ◽  
Wide Range ◽  
Increase Risk ◽  
Behavioral Mechanisms

A growing literature suggests that exposure to adverse social conditions may accelerate biological aging, offering one mechanism through which adversity may increase risk for age-related disease. As one of the most extensively studied biological markers of aging, telomere length (TL) provides a valuable tool to understand potential influences of social adversity on the aging process. Indeed, a sizeable literature now links a wide range of stressors to TL across the life span. The aim of this article is to review and evaluate this extant literature with a focus on studies that investigate psychosocial stress exposures and experiences in early life and adulthood. We conclude by outlining potential biological and behavioral mechanisms through which psychosocial stress may influence TL, and we discuss directions for future research in this area.

scholarly journals Corticolimbic Circuit Structure Moderates an Association Between Early Life Stress and Later Trait Anxiety

2019 ◽  
Author(s):  
M. Justin Kim ◽  
Madeline J. Farber ◽  
Annchen R. Knodt ◽  
Ahmad R. Hariri
Keyword(s):  
Trait Anxiety ◽  
Life Stress ◽  
Early Life ◽  
Emotional Reactivity ◽  
Early Life Stress ◽  
Childhood Adversity ◽  
Structural Features ◽  
Individual Variability ◽  
Future Research ◽  
Wide Range

AbstractChildhood adversity is associated with a wide range of negative behavioral and neurodevelopmental consequences. However, individuals vary substantially in their sensitivity to such adversity. Here, we examined how individual variability in structural features of the corticolimbic circuit, which plays a key role in emotional reactivity, moderates the association between childhood adversity and later trait anxiety in 798 young adult university students. Consistent with prior research, higher self-reported childhood adversity was significantly associated with higher self-reported trait anxiety. However, this association was attenuated in participants with higher microstructural integrity of the uncinate fasciculus and greater thickness of the orbitofrontal cortex. These structural properties of the corticolimbic circuit may capture a neural profile of relative resiliency to early life stress, especially against the negative effects of childhood adversity on later trait anxiety. More generally, our findings highlight the potential utility in the simultaneous consideration of qualitatively different brain structural measures in explaining complex behavioral associations in future research.

Air quality and mental health: evidence, challenges and future directions

2021 ◽  
Author(s):  
Kamaldeep Bhui ◽  
Joanne Newbury ◽  
Rachel Latham ◽  
Marcella Ucci ◽  
Zaheer Nasar ◽  
...  
Keyword(s):  
Mental Health ◽  
Air Pollution ◽  
Air Quality ◽  
Life Course ◽  
Evidence Base ◽  
Future Research ◽  
Knowledge Gaps ◽  
Methodological Challenges ◽  
Wide Range ◽  
The Life Course

AbstractPoor air quality is associated with poor health. Little attention is given to the complex array of environmental exposures and air pollutants that impact mental health during the life course. By gathering expertise across the air pollution and mental health fields, we summarise the findings of a rapid scoping discussion, to identify knowledge gaps and methodological challenges.. We summarise the key scientific findings, and identify knowledge gaps and methodological challenges. We propose future research priorities and the optimal methods to address them. There is emerging evidence of associations between poor air quality, both indoors and outdoors, and poor mental health and specific mental disorders. Evidence of critical periods in exposures among children and adolescents highlights the need for for more longitudinal data as the basis of early prevention policies. Particulate matter, including bioaerosols, are implicated, but form part of a complex exposome influenced by; geography, deprivation, socio-economic conditions, and biological and individual vulnerabilities. Critical knowledge gaps need to be addressed so that dedicated actions can be taken to design interventions for mitigation and prevention, reflecting ever-changing sources of air pollution. In the interim, the existing evidence base can help motivate the efforts of researchers, practitioners, policy-makers, industry, community groups, and campaigners to raise awareness and take informed action. Such work necessarily requires collaboration between a wide range of specialists. There are knowledge gaps and a need for a more substantial evidence base, for example, around bioaerosols exposure, indoor and outdoor pollution, and the mental health impacts over the life course.

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