Aging-associated diseases

Summary

An aging-associated disease (commonly termed age-related disease, ARD) is a disease that is most often seen with increasing frequency with increasing senescence. They are essentially complications of senescence, distinguished from the aging process itself because all adult animals age (with rare exceptions) but not all adult animals experience all age-associated diseases. The term does not refer to age-specific diseases, such as the childhood diseases chicken pox and measles, only diseases of the elderly. They are also not accelerated aging diseases, all of which are genetic disorders. Examples of aging-associated diseases are atherosclerosis and cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases exponentially with age. Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrializ

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https://en.wikipedia.org/wiki/Aging-associated_diseases

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The physical ends of chromosomes, known as telomeres, protect chromosome ends from nucleolytic degradation and DNA repair activities. Conventional DNA replication enzymes lack the ability to fully replicate telomere ends. In addition, nucleolytic activities contribute to telomere erosion. Short telomeres trigger DNA damage checkpoints, which mediate cellular senescence. Telomere length homeostasis requires telomerase, a cellular reverse transcriptase, which uses an internal RNA moiety as a template for the synthesis of telomere repeats. Telomerase elongates the 3' ends of chromosomes, whereas the complementary strand is filled in by conventional DNA polymerases. In humans, telomerase is ubiquitously expressed only during the first weeks of embryogenesis, and is subsequently downregulated in most cell types. Correct telomere length setting is crucial for long-term survival. The telomere length reserve must be sufficient to avoid premature cellular senescence and the acceleration of age-related disease. On the other side, telomere shortening suppresses tumor formation through limiting the replicative potential of cells. In recent years, novel insight into the regulation of telomerase at chromosome ends has increased our understanding on how telomere length homeostasis in telomerase-positive cells is achieved. Factors that recruit telomerase to telomeres in a cell cycle-dependent manner have been identified in Saccharomyces cerevisiae. In humans, telomerase assembles with telomeres during S phase of the cell cycle. Presumably through mediating formation of alternative telomere structures, telomere-binding proteins regulate telomerase activity in cis to favor preferential elongation of the shortest telomeres. Phosphoinositide 3-kinase related kinases are also required for telomerase activation at chromosome ends, at least in budding and fission yeast. In vivo analysis of telomere elongation kinetics shows that telomerase does not act on every telomere in each cell cycle but that it exhibits an increasing preference for telomeres as their lengths decline. This suggests a model in which telomeres switch between extendible and nonextendible states in a length-dependent manner. In this review we expand this model to incorporate the finding that telomerase levels also limit telomere length and we propose a second switch between a non-telomerase-associated "extendible" and a telomerase-associated "extending" state.

Springer-Verlag2006

NAD(+) homeostasis in health and disease

Johan Auwerx, Dina Hofer, Elena Katsyuba, Mario Romani

The conceptual evolution of nicotinamide adenine dinucleotide (NAD(+)) from being seen as a simple metabolic cofactor to a pivotal cosubstrate for proteins regulating metabolism and longevity, including the sirtuin family of protein deacylases, has led to a new wave of scientific interest in NAD(+). NAD(+) levels decline during ageing, and alterations in NAD(+) homeostasis can be found in virtually all age-related diseases, including neurodegeneration, diabetes and cancer. In preclinical settings, various strategies to increase NAD(+) levels have shown beneficial effects, thus starting a competitive race to discover marketable NAD(+) boosters to improve healthspan and lifespan. Here, we review the basics of NAD(+) biochemistry and metabolism, and its roles in health and disease, and we discuss current challenges and the future translational potential of NAD(+) research.

NATURE PUBLISHING GROUP2020

Increased life expectancy goes hand in hand with a higher incidence of age-related diseases that affect the nervous and metabolic systems, such as type 2 diabetes, cancer, Parkinson’s and Alzheimer’s disease. These complex diseases are a product of the combined actions of large networks of genes, and environmental factors, such as diet, exercise, drug use, and levels of acute and chronic stress. One of the main challenges in biomedical research is determining how these factors interact to influence human healthspan, in order to develop effective strategies for the diagnosis, prevention, and treatment of these chronic multifactorial diseases. A strategy that has emerged in the last decade is the modulation of mitochondrial function. Accumulating evidence support the involvement of mitochondrial dysfunction in the pathogenesis of type 2 diabetes, Parkinson’s disease, cancer, and to a lesser extent, Alzheimer’s disease. Mitochondrial processes are regulated by a highly dynamic and complex network of enzymes and transcription factors. One of the best characterized branches of this network is the AMPK/SIRT1 pathway and its downstream effectors. Recently, additional pathways important for the regulation of mitochondrial function have been described such as mitochondrial fusion and fission, specific autophagy of mitochondria, termed mitophagy, and mitochondrial unfolded protein response (UPRmt). These recent discoveries have extended the scope of potential therapeutic targets. This thesis describes the development of two complementary approaches to identify novel genetic and pharmacological determinants of mitochondrial function. 1. The first approach aims to identify novel genetic determinants of the regulatory networks that control metabolism in general, and mitochondrial function in particular, by using the mouse BXD genetic reference population (GRP). Chapter II summarizes the analysis of 140 metabolic traits in 42 BXD strains, and demonstrates the suitability and usefulness of the BXD GRP for the identification of genetic regulators of metabolism. 2. The second approach is focused on the development of pharmacological tests for the identification and characterization of novel drugs that modulate mitochondrial phenotypes. Chapter III presents the establishment and validation of a platform of mitochondrial assays in two species, i.e. mammalian cells and the worm C.elegans. A successful example of its use is shown in chapter IV, where the role of copper in tumorigenesis is elucidated by applying these mitochondrial assays Altogether, these two synergistic approaches pave the way that will lead to the identification of novel key factors and treatments for mitochondrial diseases and pathologies associated with mitochondrial dysfunction.

EPFL2013

Springer-Verlag2006