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BIOL 355 Midterm Review

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Cheryl Duxbury

BIOL 355 – Biology of Human Aging Lectures 1-14 Midterm Review Introduction  Gerontology: study of the aging process, from maturity to death. Consists of biological aging, psychological aging, and social aging (also environmental, economic, cultural and spiritual).  Gerontologist: uses multidisciplinary concepts to study all aspects of aging process  Geriatrics: branch of specialized medicine  Geriatrician: concerned with health, care, diseases, and treatment of older adults.  Biogerontology: field that studies the biological aspects of aging (physical changes in tissues, organs and systems that lead to changes in appearance and functional capacity).  Chronological aging: passage of time from birth for that individual; good for population studies. o Poor indicator of biological age because it is based on time only, arbitrary, relative and subjective. o Young-old: 60-74 o Old-old: 75-84 o Oldest-old: 85+  Biological aging: based on functional capacity; good for individuals. o Functional capacity is measure of the ability of our cells, tissues, and organ system to function optimally. o Diverse because of varied onset of aging, rate which it progresses, and extent to which it progresses. o Influenced greatly by extrinsic factors, lesser by intrinsic factors (more environment than genetics). o Extrinsic factors (control over): lifestyles/nutrition, environment, medical advancements o Intrinsic factors (no control over): genetics o Defined by 4 different criteria  Decline of functional properties  Loss of homeostasis  Decreases ability to adapt to stimuli  Increased vulnerability to disease and mortality  Normal biological aging: structural elements within the body deteriorate. Leads to loss of functional capacity and decreased ability to adapt to internal and external stressors. The reduced capacity to respond to changing internal and external environments; loss of homeostasis. Loss of homeostasis leads to an increased likelihood of disease and death. o Loss of functional capacity in cells, tissues, and organs: brain and liver weight decreases, BMR decreases, cardiac output decreases, respiratory capacity decreases. A lifetime of stress, wear and tear and degradation of cells without being replaced affects organ functions. o Loss of homeostasis: when relative constancy is disturbed (compensation for stressor fails), our cells are not operating in an optimal environment and cannot function to their maximum potential. o Biological aging causes change to structures and to negative feedback that allow more rapid or extreme alteration in body conditions; leads to decrease detection and response. o Decreased ability to handle stressors: response to stress depends on many factors (age, health, type, persistence). Adequate responses to stress include mobilizing energy, activating defense mechanisms, repairing damage.  Frailty: state of vulnerability to poor resolution of homeostasis after a stressor event; consequence of cumulative decline in many systems  Longevity: duration of life. o Maturation (birth-18yrs): growth and development, acquire new functions, perfect acquired functions, changes are beneficial o Maturity (18-30yrs): period of stabilization o Senescence (30yrs and beyond): no growth or development, changes are deleterious Aging Demographics and Trends  Aging Demographics: o More people are now 65+ than under 25 o Populations in which 10% is aged 65+ is considered old; Canada is at 15% o Fastest growing segment is 85+ o A steady increase in number of centenarians; aged 100+  Four reasons for increased elderly population: o Baby Boomers are now 65+ o Decrease in infant mortality o Increase in life expectancy (due to medical advances, public health) o Decrease in birth rates (less young people)  Life span: the age at death the longest lived individual of a species; fixed for each species  Life expectancy: the average age at which death occurs for members of the population; varied; can be from birth or any age (ex birth – LE is 85 years; at age 50 – LE is 30 years) o Historical period which you were born and lived: In Ancient Rome LE was 22 years o Country in which you live: Some third world countries have a lower LE of about 40 o Gender: Women consistently outlive men by 5-7 years  Age-independent mortality: deaths by chance; occur at any time; not related to a person’s age o Acute illness, accidents, overdoses, murder, suicide, war, disaster  Age-dependent mortality: increased risk of dying with increased age; progressive, natural impairments to cellular function and tissues which causes an increase in age- specific death rate; death due to biological processes o Chronic disease in the elderly, natural deaths  Premature deaths: large, devastating challenges the body cannot overcome, even with proper organ function o Accidents, overwhelming infection, cancer  If you cured all disease, years of life could be added. If you could slow the natural aging process, you can reach maximum life span.  Demographics of population: statistical study of human populations including size, density, geography of population; vital statistics on birth, death, disease, marriages. o Cohorts of people (~100 000) are followed from birth to death o Type 3 Survivorship Curve: can see a rectangularization from more people living longer. Increase in life expectancy is due to reductions in infant, maternal and early childhood mortality; medical advances, nutrition, technology, sanitation, socioeconomic and environmental factors. Gains are less in increasing total years lived because we do not have as much success eradicating chronic diseases. o Non-Aging Survivor Curve: for primitive populations; same risk of death every year (50%); animals do not live long enough in the wild to show signs of aging due to predation, disease, habitat, starvation, accidental death. Ancient Romans would be considered a non-aging population, as their life expectancy was only 22. o The “Ideal” Type 3 Survivorship Curve: where people die from natural causes; accident free, disease free, and violence free. Even in an ideal survivorship, we will see a brief downward turn for infant mortality. We still have stillborn babies, genetic abnormalities and malfunctioning that we can’t eradicate in utero, we will still have a small amount of infant mortality. After that, we have a huge flat line indicating a complete lifespan of 75-100 where majority of the deaths are a downward turn around 85. We have a small amount of survivors into 100-110 and that’s why we get that flat tail at the end. It would be as significant as the infant mortality – not a lot. Most people would live a full life. o We are a population that has switched from deaths from acute infectious diseases to chronic diseases.  Aging – “CUPID” – Cumulative, Universal, Progressive, Intrinsic, Deleterious  Disease – “TSDIEOD” – Treatable, Selective, Discontinuous, Intrinsic/Extrinsic, Occasionally Deleterious  Aging is not a disease.  Morbidity: increased incidence of disease with increased age. The condition where an individual is so mentally or physically disabled by chronic diseases that they become immobile or dependent on care of others.  Comorbidity: death due to multiple diseases  Acute Disease: o Leading cause of premature death o Rapid onset o Fast deterioration in health o Short term (<6 weeks) o Infectious disease o Curable  Chronic Disease: o Most resemble normal aging o Long term (>6 weeks) o Persistent and get worse with time o Not curable o Not contagious o Gradual deterioration of health o Progressive, occur in incremental steps o Clinical Threshold: disease may develop for many years before symptoms are shown o Progressive loss in organ function  Progression of Chronic Disease: o Cellular changes: undetectable minor changes to cells o Tissue changes: microscopically visible damage o Asymptomatic: detected by lab test o *Reached Clinical Threshold* o Disease symptom: progression to disability o Disability or death  Exponential increased risk of chronic disease as age increases; accidents are relatively stable then increase because it is not necessarily age-dependent.  Greatest drops in cardiovascular disease due to public health and awareness.  Rates of diseases that do not necessarily cause mortality (hypertension, arthritis, chronic bronchitis, liver disease, kidney disorders, etc.) give an idea of health of the older population by looking at comorbidity.  Top 5 Causes of Death Ages 15-34: o Accidents o Homicide (male)/cancer (women) o Suicide o Cancer (male)/homicide (female) o Heart disease  Top 5 Causes of Death Ages 55-74: o Heart disease o Cancer o Stroke o Accidents (male)/diabetes (female) o COPD (male)/accidents (females)  Cannot “cure” chronic disease; we can analyze risk factors in order to devise a strategy to slow the rate of progression and therefore postpone the disease. Cellular Changes  Chemical level  cellular level  tissue level  organ system level  organism level  Since aging is universal (CUPID) and all humans have 4 macromolecules in common, it is thought that changes in these macromolecules could cause aging  The Cell: the basic unit of life that contains enzymes and chemicals for anabolism (building material) and catabolism (burning energy). Cells have different roles and the roles are specified by different proteins and genetic information found in the nucleus. o Plasma membrane: fluid mosaic model; phospholipid bilayer with many embedded proteins that carry out specific functions. It is selectively permeable. o Proteins for transport (ionic channels that will allow things to pass through) o Cell-cell recognition (depicts majority of carbohydrates and sugars, predominantly on outside of plasma membrane or outside of organelle membrane) – reach out, test environment, communicate from cell to cell. o Communication between proteins – Receptors and ligands. Ligands can bind carbohydrates, hormones, etc. o Enzymes: majority of proteins will be enzymes. If they bind to ligand they will initiate a reaction. o Tagging: cell-identification, for a cell to go to a specific tissue. These proteins will have unique tags to go to a designated area. o Tissue/Cell Specificity: propriety, detection from immune system o Glycoproteins: used for specificity markers; signal what type of cell they are on and who they belong to (identity)  Cytoplasm: contains organelles, proteins, and inclusions (glycogen, fats, pigments).  Organelles: small organs in the cell o Endoplasmic reticulum: folded membrane system that is continuous with nucleus. Rough ER has ribosomes attached for protein synthesis. Smooth ER is for lipid and steroid synthesis and carbohydrate and toxin metabolism. o Ribosomes: attached to RER or free; composed of rRNA and protein; synthesize proteins o Mitochondria: “powerplant”; burns fuels to make energy o Lysosomes: “garbage can”; contains digestive enzymes to break down old cells and foreign particles and recycle macromolecules and organelles o Golgi apparatus: “traffic director”; final processing of new proteins by attaching glycolipid markers to tell them where to go and are packaged into vesicles o Nucleus: nuclear membrane surrounds genetic material (DNA or chromosomes) o Chromosomes: fibres of DNA, contains genetic information for protein synthesis and therefore cell function on genes.  Protein o 20 different amino acids can be arranged in infinite sequences o Conformation (unique structure of bends, folds and twists) is key to specificity and function of cell o Primary: linear sequence of amino acids (polypeptide chain) o Secondary: alpha helix or beta sheet of two polypeptide chains o Tertiary: multiple helices and sheets folded together o Quarternary: globular protein o Structural proteins: usually linear and insoluble, stable. Provide mechanical strength to tissues (collagen, keratin, elastin) o Functional proteins: globular, water soluble, active and play major roles in biological processes. Enzymes (biological catalysts) and haemoglobin (functional protein). o DNA  protein: the order of nucleotides in the gene dictates the amino acid sequence of the primary protein.  Transcription: occurs in nucleus; order of bases in DNA determines order of amino acids in mRNA  Translation: occurs in cytoplasm; mRNA takes information to ribosomes where proteins and synthesized. The specific amino acid sequence codes for a specific protein. Theories of Aging  Types of Cells in Body: o Continuously mitotic: divide and produce new cells throughout lifespan; rate does decrease with age. Bone marrow, epithelium, skin, fibroblast cells. o Post mitotic: divide during embryogenesis then stop. Nerve cells, muscle cells, brain tissue. o Semi mitotic: only divide when injured. Liver cells.  Human bodies consist of o Cells  Germ cells: egg, sperm; haploid  Somatic cells: non-gamete cells; diploid o Matrix: non-cellular, for support  To be a valid theory it must account for: Universal, Progressive, Deleterious (CUPID)  Programmed Theories: o Programmed Longevity: aging is result of sequential turning off and on of certain genes. Longevity assurance genes when on increase LE; deleterious genes when on decrease LE. o Endocrine Theory: biological clocks act through hormones to control pace of aging o Immunological Theory: a programmed decline in immune system functions leads to increased vulnerability to infectious disease and consequently, death.  Error Theories: o Wear and Tear: vital parts of cells wear out o Rate of Living: the greater the rate of oxygen metabolism, the shorter the lifespan o Crosslinking: an accumulation of cross-linked proteins damages cells, free radicals, AGE products (when AGE products bind to receptors (RAGE), they contribute to some chronic inflammatory diseases) and waste accumulation (lipofuscin – product of oxidation of unsaturated fatty acids from lysosomes). o Free Radicals: accumulated damage caused by oxygen radicals causes cells to stop functioning (unpaired electrons pull electrons off other molecule, causing it to become a free radical, etc; causes DNA crosslinking which contributes to cancer and other diseases of aging) o Somatic DNA Damage: genetic mutations occur and accumulate with increasing age. Damage to mitochondrial DNA might lead to mitochondrial dysfunction. Faulty repair to damaged DNA with age; errors in proteins with age.  Evolutionary Theories: o The purpose of a species is to prevail by creating progeny so it must maintain itself through reproduction. There is no need to invest in biological resources after they have nurtured offspring. When we are most protected and have lowest death rate is at puberty – when we become reproductive and are able to pass on genes to offspring. At age ~30, there is no more need to biologically maintain organism so we’ve lost protection, remain neutral, and start to degrade. o Mutation Accumulation: “late-acting” gene because deleterious effects are only expressed after age of reproduction. Can be an accumulation of mutations or a mutant gene is turned on. Not selected against because they do not affect reproduction or nurture the next generation. o Antagonistic Pleotrophy: Pleotrophy is when a single gene can have multiple effects. Late-acting genes may exist and have not been selected against because they have a positive effect early in life. Ex estrogen, ApoE4 (media
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