Books

Evolutionary theory and experimental tests of senescence, including age-specific natural selection, genetic mechanisms, comparative biology and evolutionary interpretations of organismal, cellular and molecular aging theories.

DNA damage and repair in mitotic and post-mitotic cell aging, including mutation rates, genomic instability, telomere dynamics, Werner syndrome, apoptosis, species lifespan, and age-dependent disease.

A biodemographic framework for aging, lifespan, mortality, reproduction, and late-life mortality patterns, drawing on large-scale fruit-fly life-table research and relating it to human aging.

Molecular damage and cellular maintenance in aging, including oxidative DNA and protein damage, genomic instability, mitochondrial free-radical biology, telomeric damage, proteasome function, lysosomal degradation, gene silencing, and transcriptional dysregulation.

Human cellular aging from genes to tissue pathology, centered on telomere maintenance, telomerase, cell senescence, progeroid syndromes and the contribution of senescent cells to age-related disease.

DNA repair fidelity and the molecular basis of hereditary disorders caused by defects in distinct DNA-repair pathways and overlapping DNA-metabolism activities.

Inflammation, nutrition, oxidation, infection, energy balance, genetics, evolution, and their effects on human aging, chronic disease, and lifespan.

Telomere and telomerase biology in aging, regeneration, cancer, adult stem-cell decline, molecular damage, checkpoint responses, metabolism, organ maintenance, and potential regenerative and anticancer therapies.

Somatic DNA mutation, genomic instability, genome maintenance, functional genomics, and systems-level evidence for damage to the genome as a cause of aging and age-related disease.

Conserved longevity mechanisms from yeast to humans, including lifespan-extending mutations, dietary restriction, mTOR, insulin and IGF signaling, comparative biology, and markers of successful aging.

Age-associated immune change across innate and adaptive cells, stem cells, genetics, signaling, mitochondria, proteasomes, cytokines, inflammation, thymic aging, clinical disease, vaccination, nutrition, and possible interventions.

Oxidative and inflammatory damage, redox regulation, cellular senescence, nuclear DNA, advanced glycation, sirtuins, mitochondria, and age-related cardiovascular and neurological disease.

Cross-species comparison of biological and molecular aging, spanning cells, organelles, tissues, organs, systemic change, and interventions that delay or accelerate aging.

Proteostasis in aging, including protein synthesis fidelity, repair, post-translational modification, degradation, turnover, autophagy, mitochondrial quality control, reactive oxygen species, dietary restriction, and lifespan regulation.

Calorie restriction as a regulator of healthspan and lifespan, integrating molecular, cellular, organismal, and clinical evidence on metabolism, stress responses, age-related disease, and dietary interventions.

Protein misfolding, aggregation, endoplasmic-reticulum and mitochondrial stress, chaperones, autophagy, quality-control responses, premature-aging connections, disease mechanisms, and laboratory methods for studying proteotoxic stress.

Extracellular-matrix structure, regulation, assembly, and remodeling across collagen, basement membranes, fibronectin, proteoglycans, hyaluronan, microfibrils, elastin, fibulins, matricellular proteins, cell-matrix receptors, and disease.

Autophagy machinery and regulation, lysosomal and endosomal fusion, selective clearance of organelles and protein aggregates, mitophagy, autophagic flux, disease mechanisms, drug discovery, aging, calorie restriction, and cellular quality control.

An integrated molecular account of cell aging connecting telomeres, DNA damage, oxidative stress, epigenetics, intracellular protein homeostasis, nutrient effects, lifespan-extending genes, and age-associated disease.

Laboratory methods for studying morphological, biochemical, and functional manifestations of cellular senescence across model organisms, including population analysis and high-throughput approaches.

Maintenance of genome stability through homologous recombination, double-strand-break repair, single-strand annealing, gene conversion, break-induced replication, sister-chromatid repair, meiotic recombination, nonhomologous end joining, DNA-damage checkpoints, and genome instability.

Comparative lifespan and senescence across animals, plants and fungi, integrating heredity, environmental effects, natural selection, life-history pace, programmed cell death and candidate mechanisms of aging.

Mitochondrial dysfunction in organismal aging and degenerative disease, with molecular and cellular perspectives on mitochondrial maintenance, damage, signaling, and pathology.

Telomere and telomerase biology, telomere replication and end protection, telomere biology disorders, stem cells and reprogramming, aging dynamics, epidemiology, bone-marrow failure, dyskeratosis congenita, cancer, and telomere-linked liver and lung disease.

The geroscience hypothesis: molecular and cellular aging as a malleable risk factor for chronic disease, with links to cancer, cardiovascular disease, neurodegeneration, diabetes, kidney disease, osteoporosis, and other conditions.

Genetic and epigenetic determinants of longevity, including DNA-damage mechanisms, whole-genome sequencing, genome-wide association studies, phenotype-genotype analysis, statistical genetics, and computational biology.

Mechanisms and consequences of stem-cell aging across model organisms and mammalian tissues, including hematopoietic, intestinal, skin, muscle, mesenchymal, and germline stem cells, stem-cell niches, age-related disease, and rejuvenation.

Molecular and cellular mechanisms of aging, centenarians, progeria and genome instability, induced pluripotent stem cells, longevity pathways in yeast and nematodes, metabolism, oxidative stress, calorie restriction and brain aging.

Sirtuins as NAD-dependent metabolic sensors controlling metabolism, stress responses, healthspan, aging, and lifespan, including NAD biology, mitochondrial protein regulation, circadian signaling, age-related metabolic disease, and small-molecule activation.

Molecular nutrition and nutrient sensing in aging, including mTOR and anabolic-catabolic signaling, inflammaging, epigenetics, DNA damage and repair, redox homeostasis, insulin sensitivity, telomeres, advanced glycation end products, and cellular senescence.

Lysosome biogenesis and regulation, autophagy and mitophagy, membrane repair, lipid metabolism, TFEB-mediated cellular clearance, aging-related neurodegeneration, lysosomal storage disorders, and therapeutic targeting of lysosomal pathways.

Autophagy signaling, autophagosome formation and physiological functions across scales, including roles in aging, neurodegeneration, immunity and cell differentiation.

Mitochondrial structure, genetics, signaling, quality control and degradation in the aging brain and in Parkinson's disease, Alzheimer's disease, multiple sclerosis and other neurodegenerative disorders.

Molecular mechanisms and biomarkers of aging and age-related disease, with particular coverage of mitochondrial dysfunction, oxidative stress, microRNAs, cellular senescence, metabolism, and neurodegeneration.

Advanced glycation end products, protein racemization, telomere shortening, mitochondrial DNA mutations, and epigenetics as connected mechanisms in aging, age-related disease, and biological-age estimation.

Evolutionary theories of senescence and comparative evidence across animals, plants and microbes, including taxa that show negligible, negative or otherwise atypical patterns of demographic aging.

Mitochondrial metabolism, mitohormesis, dynamics in aging stem cells, mitochondrial proteostasis, mtDNA mutations, sirtuins, NAD metabolism, mitophagy, calcium transport, and longevity.

Advanced glycation end products in food and tissues, including their chemistry, measurement, cellular mechanisms, clearance, inflammatory and oxidative effects, roles in aging and chronic disease, and experimental dietary or pharmacological interventions.

Systems biology, noncoding RNA, epigenetic regulation, ApoE, Hsp90 and proteostasis, adult and hematopoietic stem-cell aging, microbiota, tissue aging, biomarkers and experimental interventions.

Subcellular aging in human cells, including mitochondrial aging, protein homeostasis, genetic processes, reactive oxygen species, inflammation, nutrition, vitamins, minerals, and microbiological influences.

Genetic, epigenetic, biochemical, and metabolic regulation of aging, with attention to the nervous system, immunity, stem cells, age-related disease, dietary restriction, exercise, and nutrition.

Molecular, cellular, physiological, immunological, and neurological biomarkers of human aging, including genetic markers, epigenetic clocks, immunosenescence, inflammaging, mortality prediction, and integration with clinical measures.

The basic biology of autophagy, including signaling pathways, regulatory processes, cellular homeostasis, organ function, model systems, omics methods, and roles in human disease and aging research.

Experimental methods for studying age-related changes in stem and progenitor cells, including muscle stem cells, mesenchymal-cell senescence and differentiation, clonal hematopoiesis, short telomeres, and autophagy.

The NAD+-dependent sirtuin SIRT6 in DNA-damage repair and premature aging, including lamin A regulation, p53, acetylation and lifespan phenotypes in SIRT6-deficient mice.

Oxidative stress mechanisms in aging and their interaction with mitochondrial dysfunction, cellular signaling, apoptosis, senescence, inflammation, sarcopenia, organ aging, animal models, dietary antioxidants, and redox-active nutrients.

The molecular pillars of aging viewed through genetics and genomics, including mitochondrial function, epigenetics, biomarkers, alternative splicing, progeroid disease, microbiome research and CRISPR applications.

Modern biogerontology, including multi-omics and systems approaches, longevity pathways and interventions, mTOR, genetics, evolutionary biology, bone aging, and epigenetic control.

Cellular senescence across cancer, lung, liver, kidney and vascular disease, diabetes, obesity, sarcopenia, bone and cartilage disorders, neurodegeneration, frailty, tissue aging, and senescence-directed experimental therapies.

Redox signaling and homeostasis in aging, oxidative damage biomarkers, mitochondrial and organelle redox dysfunction, autophagy, redox proteostasis, inflammation, cellular senescence, and age-related disorders.

Molecular aging of long-lived proteins, including spontaneous side-chain modifications, solubility changes, proteostasis and lysosomal degradation, Maillard chemistry, protein cross-links and age-related disease.

A unified treatment of the hallmarks of aging: DNA damage, epigenetic aging, nutrient sensing, proteostasis, mitochondrial dysfunction, NAD+ depletion, autophagy, cellular senescence, altered communication, and stem-cell exhaustion.

Mechanisms of aging and longevity across model organisms, from molecular and cellular processes to systemic physiology, metabolism, brain aging, and neurodegeneration.

Comparative biology of exceptional longevity across wild animals, including insects, birds, bats, mole rats, elephants, whales, sharks, quahogs, fish, dolphins, and long-lived marine invertebrates, with attention to evolved resistance to aging and disease.

Translating aging mechanisms into interventions, with coverage of cellular senescence, NAD+, biomarkers, autophagy, antioxidants, chemistry, clinical trials, and geroscience ethics.

Model-organism and human longevity research, including biomarkers, insulin and FOXO signaling, dietary restriction, proteostasis, mitochondria, DNA repair, reproductive aging, cognition, and the microbiome.

Subcellular aging in human cells, including microRNAs, circular RNAs, mitochondria, extracellular vesicles, gap junctions, nuclear pores, the proteasome, systems biology, and therapeutic modulation of senescence.

Mechanism-based intervention strategies including telomerase activation, stem-cell therapy, autophagy induction, sirtuin activation, epigenetic modulation, tissue engineering, regenerative medicine, dietary restriction, and associated ethics.

Experimental methods for mitochondrial-DNA isolation, imaging, nucleoid structure and packaging, replication, genome integrity, damage bypass and repair, sequencing, gene editing, disease diagnostics, and analysis of mtDNA-interacting proteins.

How health systems, economies, careers, finances, relationships, and public institutions can adapt to longer, healthier lives.

A concise science-facing overview of aging through evolution, the genome and epigenome, gene regulation, cellular mechanisms, nutrition, immunity, progeroid syndromes, cancer, and common age-related diseases.

Mechanism-based interventions targeting aging biology, including telomerase, proteasome and chaperone activation, NAD+ restoration, senolytics, stem-cell therapies, dietary restriction, SIRT1, hormesis, exercise, geroprotectors, and the gut microbiome.

A hallmark-structured account of genomic instability, telomere shortening, epigenetic change, proteostasis, mitochondrial dysfunction, stem-cell exhaustion, altered intercellular communication, SASP and cellular senescence.

Telomere DNA-protein structure, replication and length maintenance, telomerase, alternative lengthening, TERRA, telomere biology disorders and telomere-directed therapeutic research.

Cellular senescence and SASP, epigenetic changes, stem-cell exhaustion, immunosenescence, age-related disease, and therapeutic approaches including small molecules, gene therapy, and regeneration.

The evolutionary origins of human longevity, evidence from subsistence populations, chronic disease in later life, multigenerational living, and the social conditions that support healthy aging.

Autophagy machinery, cargo receptors, autophagosome formation, measurement and control of autophagic flux, chaperone-mediated autophagy, mitophagy, proteostasis, and autophagy dysfunction in aging and age-related disease.