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译，敬请等待第二版的翻译及更新，谢谢。)
第一章：衰老生物学的基本概念
1.1老年生物学（biogerontology）: 专门研究生物衰老
1.1.1 当人类寿命增加时生物学家开始研究衰老
1.1.2 在1940年代老年生物学成为一个独立的研究领域
1.1.3 当前的衰老研究致力于人的整体健康
1.1.4 其它物种的生物学衰老与人类衰老具有相同性状
1.1.5 衰老研究是一个复杂的过程
1.2 生物衰老的定义
1.2.1 生物学衰老的第一个定义是基于死亡率的
1.2.2 基于功能的定义有助于描述特殊时期的生物学衰老
1.2.3 衰老的生物学定义
1.2.4 发育，成熟和衰老是用以描述衰老与事件关联的阶段
1.2.5 生物学衰老与老年疾病是不同的
1.3 老年生物学家们怎么研究衰老：用实验室生物体研究人类衰老
1.3.1 分离的细胞系统可被用来研究衰老和寿命的基本生物化学
1.3.2 真菌是研究影响衰老和寿命的环境因子的理想材料
1.3.3 原始无脊椎动物可能提供细胞寿命延长的线索，细胞信号和整体衰老
1.3.4 昆虫可用于研究how whole-body and 细胞内 signaling affect life history
1.3.5 在调查营养，遗传和生理问题上，小白鼠是最常见的实验材料
1.3.6 Nonhuman primates display many of the same time-dependent changes as humans
1.3.7 Human progerias can be used to model normal human aging
1.4 老年生物学家们怎么研究衰老：比较老年生物学
1.4.1 物种的身体尺寸与最大寿命是相关联的
1.4.2 Reduced vulnerability to extrinsic dangers explains extended 寿命
1.4.3 A highly organized social structure also extends 寿命 in the wild
1.4.4 A few aquatic animals have extreme 寿命
第二章：测量生物学衰老
2.1 MEASURING 生物学衰老 IN THE INDIVIDUAL
2.1.1 Differences in the age-related phenotype affect the measurement of aging in individuals
2.1.2 Lifestyle choices significantly affect phenotype
2.1.3 The表观基因组can also affect the rate of aging and 寿命
2.1.4 Cross-sectional studies compare changes in different age groups at a single point in time
2.1.5 Longitudinal studies observe changes in a single individual over time
2.1.6 Personal genomics will probably be the key to determining and applying biomarkers for aging
2.2 MEASURING 生物学衰老 IN A POPULATION
2.2.1 Mortality rates estimate the number of deaths in populations
2.2.2 Life tables contain information on mortality, life expectancy, and the probability of dying
2.2.3 Age-specific mortality rate rises exponentially
2.2.4 Age-independent mortality can affect the mortality rate
2.2.5 Mortality-rate doubling time corrects for differences in initial mortality rates
2.2.6 Survival curves approximate mortality rate
2.2.7 Deceleration of mortality rate at the end of life suggests the possibility of 寿命 genes
第三章：寿命和衰老的进化理论
3.1 FOUNDATIONS OF EVOLUTIONARY THEORIES OF 寿命 AND AGING
3.1.1 Weismann established the separation between soma and germ cells
3.1.2 Weismann proposed that aging is a nonadaptive trait
3.1.3 Population biologists developed logistic equations to calculate population growth
3.1.4 A population’s age structure describes Darwinian fitness in complex eukaryotes
3.1.5 Reproduction rate describes age-specific fitness in breeding populations
3.1.6 Fisher described the relationship between reproductive potential and Darwinian fitness in
Populations
3.2 EVOLUTION AND 寿命
3.2.1 The extrinsic rate of aging leads to a decline in the force of natural selection
3.2.2 Medawar theorized that aging arose as a result of genetic drift 66
3.2.3 Medawar proposed that aging and 寿命 arise separately in postreproductive populations
3.2.4 Hamilton’s force of natural selection on mortality refined Medawar’s theory
3.3 TESTING EVOLUTIONARY MODELS OF 寿命
3.3.1 Late-reproducing organisms have a lower rate of intrinsic mortality
3.3.2 Genetic drift links life span to reproduction
3.3.3 Results from testing the evolutionary theory of 寿命 have changed research in 老年生物学
3.4 进化和衰老
3.4.1 Antagonistic pleiotropy is a special case of general pleiotropy
3.4.2 The disposable soma theory is based on the allocation of finite resources
第四章：细胞内衰老
4.1 细胞周期和细胞分裂
4.1.1 The cell cycle consists of four phases plus one
4.1.2 DNA replication occurs during the S phase
4.1.3 Cell division occurs during the M phase
4.2 REGULATION OF THE CELL CYCLE
4.2.1 S-cyclins and cyclin-dependent kinases initiate DNA replication
4.2.2 The p53 pathway can prevent DNA replication at the G1-to-S phase transition
4.2.3 Many proteins are involved in the replication of DNA
4.2.4 Cohesins and condensins help control chromosome segregation
4.2.5 The metaphase-to-anaphase transition marks the final checkpoint in the cell cycle
4.2.6 Fully functional cells can exit the cycle at the G0 phase
4.3 REPLICATIVE SENESCENCE
4.3.1 A mistake delayed the discovery of cell senescence for 50 years
4.3.2 Hayflick and Moorhead’s research findings created the field of cytogerontology
4.3.3 Cells in culture have three phases of growth
4.3.4 Senescent cells have several common features
4.3.5 Replicative senescence can be used to describe 生物学衰老
4.4 引起细胞衰老的原因：被破坏的生物分子的积累
4.4.1 Biomolecules are subject to the laws of thermodynamics
4.4.2 Life requires the constant maintenance of order and free energy
4.4.3 The mechanism underlying aging is the loss of molecular fidelity
4.4.4 Aging reflects the intracellular accumulation of damaged biomolecules
4.5 OXIDATIVE STRESS AND CELLULAR AGING
4.5.1 Oxidative metabolism creates reactive oxygen species
4.5.2 Mitochondrial ATP synthesis produces the majority of superoxide ions Enzymes catalyze reduction of the superoxide radical to water
4.5.3 Cytosolic reduction also generates free radicals
4.5.4 Oxygen-centered free radicals lead to the accumulation of damaged biomolecules
4.5.5 Cell membranes are susceptible to damage by reactive oxygen species
4.5.6 Reactive oxygen species can have beneficial effects
4.6 TELOMERE SHORTENING AND REPLICATIVE SENESCENCE
4.6.1 Telomeres prevent the lagging strand from removing vital DNA sequences
4.6.2 Shortening of the telomere may cause somatic cell senescence
第五章：寿命的遗传学
5.1 真核生物基因表达预览
5.1.1 Transcription of DNA produces complementary RNA
5.1.2 Eukaryotic cells modify RNA after transcription
5.1.3 Translation is the RNA-directed synthesis of a protein
5.1.4 Proteins can be modified or degraded after translation
5.2 基因表达的调节
5.2.1 Gene expression can be controlled by changing nucleosome structure
5.2.2 Gene expression is controlled by binding of proteins to DNA
5.2.3 Post-transcriptional mechanisms can also control gene expression
5.3 ANALYZING基因表达IN 老年生物学
5.3.1 Genetic analysis in 老年生物学 begins with the screening of mutants
5.3.2 Identification of gene function requires DNA cloning
5.3.3 The function of the gene can be partially determined from its sequence
5.3.4 In situ hybridization can reveal a gene’s function
5.3.5 Genetically altering organisms helps evaluate a gene’s impact on human 寿命
5.3.6 DNA microarrays are used to evaluate gene expression patterns at different ages
5.4 GENETIC REGULATION OF 寿命 IN S. CEREVISIAE
5.4.1 S. cerevisiae reproduces both asexually and sexually
5.4.2 Environmental conditions influence reproduction and life span
5.4.3 Structural alteration in DNA affects life span
5.4.4 The SIR2 pathway is linked to 寿命
5.4.5 Loss-of-function mutations in nutrient-responsive pathways may extend the life span
5.5 GENETIC 调控OF 寿命 IN C. ELEGANS
5.5.1 Regulation of dauer formation extends life span
5.5.2 Genetic pathways regulate dauer formation
5.5.4 Weak mutations in the DAF-2 receptor extend life span
5.5.5 Life extension is linked to neuroendocrine control
5.5.6 Mitochondrial proteins may be the link between extended life span and metabolism
5.6 GENETIC REGULATION OF 寿命 IN D. MELANOGASTER
5.6.1 Drosophila has a long history in genetic research
5.6.2 Genes that extend 寿命 are associated with increased stress resistance
5.6.3 Genes controlling Drosophila’s growth also extend life span
5.7 GENETIC REGULATION OF 寿命 IN M. MUSCULUS
5.7.1 Many M. musculus genes have been reported to affect 寿命
5.7.2 Decreased insulin signaling links retarded growth to 寿命
5.7.3 Diminished growth hormone signaling links insulin-like signaling pathways to increased寿命
5.7.4 Genetic regulation of 寿命 demonstrated in mice has implications for human aging
第六章：植物衰老
6.1 BASIC PLANT BIOLOGY
6.1.1 Plant cells have a cell wall, a central vacuole, and plastids
6.1.2 Photosynthesis takes place in the chloroplast
6.1.3 Plant hormones regulate growth and development
6.2 THE BIOLOGY OF PLANT SENESCENCE
6.2.1 Mitotic senescence occurs in cells of the apical meristem
6.2.2 Post-mitotic plant senescence involves programmed and stochastic processes
6.2.3 Leaves of Arabidopsis thaliana are the model for plant senescence
6.2.4 Leaf senescence is a three-step process
6.2.5 Monosaccharides have an important role in leaf senescence
6.2.6 Breakdown of the chloroplast provides nitrogen and minerals for other plant organs
6.2.7 Catabolic by-products may stimulate expression of genes involved in organelle dismantling
6.2.8 Plant membranes degrade during leaf senescence
6.3 INITIATING PLANT SENESCENCE
6.3.1 Light intensity affects the initiation of plant senescence
6.3.2 Cytokinins delay senescence
6.3.3 Other plant hormones induce senescence
第七章：人类寿命
7.1 ORIGINS OF HUMAN 寿命
7.1.1 Human mortality rates are facultative
7.1.2 Genetic factors cause significant plasticity in human mortality rates
7.1.3 Mortality rates differ in long-lived humans
7.1.4 Human intelligence has altered mortality rates
7.1.5 Human intelligence has produced a unique 寿命 trajectory
7.1.6 Heredity has only a minor influence on human life span
7.2 THE RISE OF EXTENDED HUMAN LIFE SPAN IN THE TWENTIETH CENTURY
7.2.1 For most of human history, the average human life span was less than 45 years
7.2.2 Control of infectious diseases increased mean life span
7.2.3 Decreases in infant mortality increased life expectancy
7.2.4 Improved medical treatments account for the continuing increase in life expectancy
7.2.5 Women have a longer life expectancy than men
第八章：人类衰老的生理学
8.1 身体组成和能量代谢的变化
8.1.1 Energy balance is the difference between intake and expenditure8
8.1.2 Accumulation of fat occurs throughout maturity
8.1.3 Excessive loss of body weight near the end of the life span increases mortality rate
8.1.4 Sarcopenia is the age-related decline in skeletal muscle mass
8.2 皮肤的变化
8.2.1 皮肤包含三层
8.2.2 Wrinkles are caused by a loss of skin elasticity and subcutaneous fat
8.2.3 Ultraviolet light causes significant damage to the skin over time
8.3 感觉的变化：听力，视力，味觉和嗅觉
8.3.1 The sense of hearing is based on the physics of sound
8.3.2 Transmission of sound through the human ear occurs in three steps
8.3.3 Loss of stereocilia contributes to age-related hearing loss
8.3.4 The sense of sight is based on the physics of light
8.3.5 Presbyopia can be explained by age-related changes in the refractive power of the lens
8.3.6 Terminal differentiation of lens cells leads to the formation of cataracts
8.3.7 The senses of taste and smell change only slightly with age
8.4 消化系统的变化
8.4.1 Age-related changes in the mouth and esophagus do not impair digestion
8.4.2 Decline in stomach function is most often associated with atrophic gastritis
8.4.3 Changes in the small intestine can affect digestion and nutrient absorption
8.5 泌尿系统的变化
8.5.1 The kidneys remove metabolic waste products from the blood
8.5.2 The kidneys help regulate blood pressure
8.5.3 Renal blood flow and kidney function decline with aging
8.6 免疫系统的变化
8.6.1 Innate immunity provides the first line of defense against infection
8.6.2 Acquired immunity relies on lymphocytes reacting to antigens
8.6.3 The phagocytotic function of neutrophils and macrophages declines with age
8.6.4 The production of naive T cells, B细胞数量, and effectiveness of 抗体all decline with age
8.7 生殖系统的改变
8.7.1 Menopause is caused by declining secretion of sex hormones by the gonads
8.7.2 Male fertility declines slightly with age
8.7.3 Old age is not a barrier to sexual activity
第九章：与年龄有关的人类疾病
9.1 THE NERVOUS SYSTEM AND NEURAL SIGNALS
9.1.1 The nervous system is composed of neurons and supporting cells
9.1.2 Membrane potentials establish the conditions for neural signal transmission
9.1.3 Neurotransmitters chemically link neurons together at the synapse
9.1.4 The human brain is a collection of separate organs and cell types
9.2 与年龄有关的人类大脑疾病：阿兹海默症和帕金森症
9.2.1 Changes in structure and neurotransmission seem to be minor in the aging brain
9.2.2 Amyloid plaques and neurofibrillary tangles accumulate in the aged brain
9.2.3 阿兹海默症 is an age-related, nonreversible brain disorder
9.2.4 阿兹海默症 begins in the entorhinal cortex and progresses into the cortex
9.2.5 The ε4 allele of the apolipoprotein E gene is a risk因子for late-onset 阿兹海默症
9.2.6 Treatments for 阿兹海默症 target neurotransmission and the prevention and degradation of amyloid plaques
9.2.7 帕金森症 is associated with loss of dopaminergic neurons
9.2.8 Increasing the brain’s多巴胺浓度is the primary objective in treatment of 帕金森症
9.2.9 Lewy bodies are the pathological hallmark of 帕金森症
9.2.10 Several genes are associated with early-onset 帕金森症
9.2.11 Several factors may predispose individuals to 帕金森症
9.3 THE CARDIOVASCULAR SYSTEM
9.3.1 The cardiovascular system is a closed system of fluid transport
9.3.2 The heart and arteries are excitable tissues
9.3.3 The heart controls blood flow and pressure by adjusting cardiac output
9.3.4 Principles of fluid dynamics govern overall blood flow
9.4 与衰老相关联的心血管系统疾病：心血管疾病
9.4.1 Environmental factors influence age-related decline in the cardiovascular system
9.4.2 Arterial plaques can lead to atherosclerosis and ischemic events
9.4.3 Risk factors for atherosclerosis are a mixture of genetic and environmental conditions
9.4.4 Statins reduce the synthesis of cholesterol in the liver and lower serum cholesterol
9.4.5 Hypertension is the most common chronic condition in the aged
9.4.6 Heart failure results in a decline in cardiac output
9.4.7 Prevalence is a better descriptor of cardiovascular disease than is mortality
9.5 内分泌系统和葡萄糖调节
9.5.1 血糖浓度must be maintained within a narrow range
9.5.2 Insulin facilitates 葡萄糖 uptake into肝脏，肌肉以及脂肪组织细胞
9.6 AGE-RELATED DISEASE OF 内分泌系统：TYPE 2 DIABETES MELLITUS
9.6.1 Insulin resistance is a precursor to type 2 diabetes
9.6.2 Type 2 diabetes impairs microvascular blood flow
9.6.3 Altered 葡萄糖 metabolism may increase cell damage in people with type 2 diabetes
9.6.4 Risk factors for diabetes include increasing age, obesity, and genetic background
9.7 THE SKELETAL SYSTEM AND BONE CALCIUM METABOLISM
9.7.1 Parathyroid and thyroid hormones balance blood calcium
9.7.2 Hormones regulate the balance between bone mineral deposition and resorption
9.8 AGE-RELATED DISEASES OF BONE: OSTEOPOROSIS
9.8.1 An increased rate of bone mineral loss at menopause can lead to osteoporosis
9.8.2 Environmental factors influence the risk of developing osteoporosis
9.8.3 Drug therapies can slow bone loss in postmenopausal women
第十章：调整人类衰老和寿命
10.1 MODULATING 生物学衰老
10.1.1 Aging cannot be modulated
10.1.2 Mechanisms that lead to loss of molecular fidelity may be modulated in the future
10.2 MODULATING 寿命: CALORIE RESTRICTION
10.2.1 Calorie restriction increases life span and slows the rate of aging in rodents
10.2.2 Calorie restriction in simple organisms can be used to investigate genetic and molecular mechanisms
10.2.3 Calorie restriction in nonhuman primates may delay age-related disease
10.2.4 The effectiveness of calorie restriction in humans remains unknown and controversial
10.3 MODULATING THE RATE OF AGING: PHYSICAL ACTIVITY
10.3.1 Exercise increases the muscles’demand for oxygen
10.3.2 Overloading cellular oxidative pathways increases the capacity for ATP synthesis
10.3.3 Regular physical activity prevents a decline in cellular reserve capacity
10.4 LOOKING TOWARD THE FUTURE: THE IMPLICATIONS OF MODULATING AGING AND 寿命
10.4.1 Extended youth and the compression of morbidity will characterize aging in the future
10.4.2 Long life may modify our perception of personal achievement and a progressive society
10.4.3 Extended 寿命 may change our responsibility for renewal of the species
10.4.4 Low birth rates and extended 寿命 may alter the current life cycle of generations
10.5 老年生物学的未来
