Contributions of Telomere Biology to Human Age-Related Disease

2016 ◽  
pp. 205-239 ◽  
Author(s):  
Ting-Lin B. Yang ◽  
Shufei Song ◽  
F. Brad Johnson
Keyword(s):  
Related Disease ◽  
Age Related ◽  
Telomere Biology

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.

Physical Activity May Improve Aging Through Impacts on Telomere Biology

2015 ◽  
Vol 4 (1) ◽  
pp. 99-106
Author(s):  
Stephen M. Roth
Keyword(s):  
Physical Activity ◽  
Mortality Rates ◽  
Cellular Aging ◽  
Critical Threshold ◽  
Telomere Shortening ◽  
Future Directions ◽  
Related Disease ◽  
Age Related ◽  
Favorable Influence ◽  
Telomere Biology

Physical activity has long been touted as a means of reducing susceptibility to age-related disease and multiple studies have shown reduced mortality rates in individuals with a lifestyle including regular exercise. A variety of mechanisms for how physical activity reduces age-related diseases have been explored and multiple, redundant explanatory mechanisms are likely to emerge. Evidence has emerged that physical activity may impact directly on telomere biology, one of the primary theories of cellular aging. Telomeres are located at the ends of chromosomes and as cells divide, incomplete DNA replication results in telomere shortening; once shortening reaches a critical threshold, cell senescence results. Investigators hypothesize that part of the favorable influence of physical activity on mortality rates and age-related disease occurs through a direct impact on telomere biology, including delaying rates of telomere shortening. The present review examines key recent findings in this area and explores some of the unanswered questions and future directions for the field.

scholarly journals Rescuing Immunosenescence via Non-Specific Vaccination

Immuno ◽  
2021 ◽  
Vol 1 (3) ◽  
pp. 231-239
Author(s):  
Alexander I. Mosa
Keyword(s):  
Immune Responses ◽  
The Elderly ◽  
Short Review ◽  
Functional Markers ◽  
Healthy Life ◽  
Related Disease ◽  
Age Related ◽  
Population Vulnerability ◽  
Mechanistic Basis ◽  
Promising Avenue

Discrepancies in lifespan and healthy-life span are predisposing populations to an increasing burden of age-related disease. Accumulating evidence implicates aging of the immune system, termed immunosenescence, in the pathogenesis of multiple age-related diseases. Moreover, immune dysregulation in the elderly increases vulnerability to infection and dampens pathogen-specific immune responses following vaccination. The health challenges manifesting from these age related deficits have been dramatically exemplified by the current SARS-CoV-2 pandemic. Approaches to either attenuate or reverse functional markers of immunosenescence are therefore urgently needed. Recent evidence suggests systemic immunomodulation via non-specific vaccination with live-attenuated vaccines may be a promising avenue to at least reduce aged population vulnerability to viral infection. This short review describes current understanding of immunosenescence, the historical and mechanistic basis of vaccine-mediated immunomodulation, and the outstanding questions and challenges required for broad adoption.

scholarly journals Genome and Epigenome Editing in Mechanistic Studies of Human Aging and Aging-Related Disease

Gerontology ◽  
2016 ◽  
Vol 63 (2) ◽  
pp. 103-117 ◽  
Author(s):  
Cia-Hin Lau ◽  
Yousin Suh
Keyword(s):  
Animal Models ◽  
Genetic Manipulation ◽  
Logic Gate ◽  
Therapeutic Interventions ◽  
Human Aging ◽  
Aging Research ◽  
Epigenome Editing ◽  
Related Disease ◽  
Age Related

The recent advent of genome and epigenome editing technologies has provided a new paradigm in which the landscape of the human genome and epigenome can be precisely manipulated in their native context. Genome and epigenome editing technologies can be applied to many aspects of aging research and offer the potential to develop novel therapeutics against age-related diseases. Here, we discuss the latest technological advances in the CRISPR-based genome and epigenome editing toolbox, and provide insight into how these synthetic biology tools could facilitate aging research by establishing in vitro cell and in vivo animal models to dissect genetic and epigenetic mechanisms underlying aging and age-related diseases. We discuss recent developments in the field with the aims to precisely modulate gene expression and dynamic epigenetic landscapes in a spatial and temporal manner in cellular and animal models, by complementing the CRISPR-based editing capability with conditional genetic manipulation tools including chemically inducible expression systems, optogenetics, logic gate genetic circuits, tissue-specific promoters, and the serotype-specific adeno-associated virus. We also discuss how the combined use of genome and epigenome editing tools permits investigators to uncover novel molecular pathways involved in the pathophysiology and etiology conferred by risk variants associated with aging and aging-related disease. A better understanding of the genetic and epigenetic regulatory mechanisms underlying human aging and age-related disease will significantly contribute to the developments of new therapeutic interventions for extending health span and life span, ultimately improving the quality of life in the elderly populations.

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