This book focuses on four of the hallmarks of aging: aspartic acid racemization, advanced glycation end products, telomere shortening and mitochondrial mutations; describing their role in aging and diseases; and their application to age-at-death estimation in forensic sciences in greater depth, displaying the interconnecting pathways among these processes. An additional chapter related to Epigenetics and its role in aging, diseases, and forensic age estimation is also included. This book is aimed at a broad audience: from students being introduced to aging, diseases, and forensic science research to scientists in biomedicine and forensics complementing their knowledge in their respective fields while also increasing their knowledge in other disciplines.

This book focuses on four of the hallmarks of aging: aspartic acid racemization, advanced glycation end products, telomere shortening and mitochondrial mutations; describing their role in aging and diseases; and their application to age-at-death estimation in forensic sciences in greater depth, displaying the interconnecting pathways among these processes. An additional chapter related to Epigenetics and its role in aging, diseases, and forensic age estimation is also included. This book is aimed at a broad audience: from students being introduced to aging, diseases, and forensic science research to scientists in biomedicine and forensics complementing their knowledge in their respective fields while also increasing their knowledge in other disciplines.

Aging of unicellular and multicellular eukaryotic organisms is a convoluted biological phenomenon, which is manifested as an age-related functional decline caused by progressive dysregulation of certain cellular and organismal processes. Many chronic diseases are associated with human aging. These aging-associated diseases include cardiovascular diseases, chronic obstructive pulmonary disease, chronic kidney disease, diabetes, osteoarthritis, osteoporosis, sarcopenia, stroke, neurodegenerative diseases (including Parkinson’s, Alzheimer’s, and Huntington’s diseases), and many forms of cancer. Studies in yeast, roundworms, fruit flies, fishes, mice, primates, and humans have provided evidence that the major aspects and basic mechanisms of aging and aging-associated pathology are conserved across phyla. The focus of this International Journal of Molecular Sciences Special Issue is on molecular and cellular mechanisms, diagnostics, and therapies and diseases of aging. Fifteen original research and review articles in this Special Issue provide important insights into how various genetic, dietary, and pharmacological interventions can affect certain longevity-defining cellular and organismal processes to delay aging and postpone the onset of age-related pathologies in evolutionarily diverse organisms. These articles outline the most important unanswered questions and directions for future research in the vibrant and rapidly evolving fields of mechanisms of biological aging, aging-associated diseases, and aging-delaying therapies.

Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.

This book provides an overview of recent advances in the study of aging and aging related diseases, discussing the topics at individual, organ, tissue, cell, and molecular levels. It also presents studies on the biomarkers of aging and anti-aging interventions. Aging has been becoming a global health problem. However it was not possible to determine aging as we usually diagnose a disease because there are few biomarkers for age estimation. Since ancient times, people have been seeking anti-aging substances and methods for achieving immortality, while the scientific study of aging has only existed for 100 years. This book appeals to researchers both in institutes and in pharmaceutical companies interested in further studies in this field.

Aging represents a physiological and per se non-pathological and multifactorial process involving a set of key genes and mechanisms being triggered by different endogenous and exogenous factors. Since aging is a major risk factor in connection with a variety of human disorders, it is increasingly becoming a central topic in biochemical and medical research. The plethora of theories on aging – some of which have been discussed for decades – are neither isolated nor contradictory but instead can be connected in a network of pathways and processes at the cellular and molecular levels. This book summarizes the most prominent and important approaches, focusing on telomeres, DNA damage and oxidative stress as well as on the possible role of nutrition, the interplay between genes and environment (epigenetics) and intracellular protein homeostasis and introduces some genes that have actually extended life spans in animal models. Linking these different determinants of aging with disease, this volume aims to reveal their multiple interdependencies. We see that there is no single “perfect” theory of aging and that instead it is possible to define what the authors call the molecular aging matrix of the cell. A better knowledge of its key mechanisms and the mutual connections between its components will lead to a better understanding of age-associated disorders such as Alzheimer’s disease.