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Unformatted text preview: GERONTOLOGY 310 PHYSIOLOGY OF AGING Fall 2009
Dr. Kelvin Davies (office hours: by appt) Dr. Christian Pike (office GER 306D: Wed 12-1, by appt) • Evaluation: two exams & term paper 1) Midterm exam: October 19 - 33% of grade - covers material from August 24 - October 14 - style: short essay questions - typically one question per lecture 2) Final exam: December 14, 8-10 AM - 33% of grade - covers material from Oct 21 - Dec 2; not cumulative - same format as the midterm 3) Term paper: due no later than December 2 - 34% of grade - in-depth review of an aspect of biology of aging - students choose own topic - requires instructor approval - email topic to instructors no later than Oct 19 - formatting details in syllabus - at least 10 pages, double-spaced - at least 10 references from scientific literature - largely journal articles - limit use of popular media, internet sites, etc. Course format
How are we going to cover the listed issues? • theoretical perspective • discuss each of the body’s systems - for each: 1. Review normal function, anatomy, physiology 2. Discuss the effects of aging on normal physiology 3. Discuss key age-related diseases in each system • emphasize differences between normal aging and disease • focus on interactions between environmental & genetic factors • discuss strategies to promote successful, healthy aging Course schedule Course
Aug. Aug. Aug. Sept. Sept Sept. Sept. Sept. Sept. Sept. Sept. Sept. Oct . Oct . Oct . Oct . Oct. 24 26 31 2 7 9 14 16 21 23 28 30 5 7 12 14 19 Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mo n. Introduction to class and structure/evaluation Aging and disease Ğ an overview Endocrine system in aging I Endocrine system in aging II LAB OR DAY HO LIDAY Ğ NO CLA SS Principles of G erontology Theories of biological aging Free Radical Th eory of aging Integument I Integument II Neu robiology of aging I Neu robiology of aging II Neu robiology of aging III Neu robiology of aging IV Skeletal system in aging Muscular system in aging MI D-TER M EXAMINA TION Kelvin D avies Kelvin D avies Kelvin D avies Kelvin D avies Kelvin D avies Christian Pike Christian Pike Christian Pike Christian Pike Kelvin D avies Kelvin D avies Kelvin D avies Christian Pike Joanna Davies Christian Pike Christian Pike Course schedule Course
Oct . Oct . Oct . Nov. Nov. Nov. Nov. Nov. Nov. Nov. Nov. Nov. Dec. Dec. 21 26 28 2 4 9 11 16 18 23 25 30 2 14 Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Wed. Mon. Heart and circulatory system in aging Respiratory systems in aging Coordination & Integration of the Cardiovascular system Sensory systems in aging I Sensory systems in aging Immune system in aging I Immune system in aging II Reproductive system in aging I Reproductive system in aging II Urinary system in aging Digestive system in aging Nutrition in aging Caloric Restriction & Aging FI NAL EXA MINA TION 8 a. m. to 10 a.m. Kelvin D avies Kelvin D avies Kelvin D avies Christian Pike Christian Pike Christian Pike Christian Pike Christian Pike Christian Pike Christian Pike Kelvin D avies Kelvin D avies Valter Longo Kelvin D avies The study of aging: examination of lifespan The
• each species has a fixed maximum lifespan (max. longevity): maximum the longest life achieved by a member of a species the - selective breeding can increase max. lifespan - human max. lifespan 120-130 years - not likely to increase bc. selective breeding not ethical not - also responsible genes not clearly known also -if/when identified many ethical, social, political, -if/when economic issues to be addressed economic - to increase, need to slow the entire aging process, to need not just age-related diseases; we don't yet sufficiently understand this process understand • mean longevity (life expectancy): mean the average age that death occurs for members of a population the - differences in mean long. used as a tool to investigate aging differences - for example,women have higher mean longevity than men. Why? for
1) hormones (estrogen, progesterone protective) 1) 2) extra X chromosome may provide imp. additional genetic material 3) women have less iron; iron generates radicals 4) traditionally, women have less risky careers 5) men may be more likely to take serious physical risks Theories of aging Theories
• many theories, none of which has been shown to be none completely correct = no complete theory on aging no • theories include: theories - general genetic theories - somatic mutation - error theory - stress theories - endocrine theories (sex hormones, pituitary) - wear and tear - cellular genetic theories (DNA damage) - free radical theories - immune theories - cross-linking - clinker theories - interaction, network Two general types of aging theories Two 1) intrinsic (aka biological clock & program theories): aging generated intentionally by the organism under the direction of some program inherent in the genetic code of the animal - aging as an extension of the embryology & maturation phases of development - aging is an active process produced internally 2) extrinsic (aka stochastic & wear and tear theories): aging is akin to wear and tear of mechanical objects. Over time, there is a decrease in function due to an accumulation of usual and unavoidable damage to tissues - aging is a passive process produced externally Lifespan correlates with length of development to adulthood • slower embryological &maturational development predict prolonged lifespan in primates - predicted if consider adulthood/aging part of development Lifespan correlates with length of sexual maturation Lifespan correlates with length of sexual maturation • if slower development predicts longer lifespan, would delaying sexual maturity increase lifespan?? Experimental delay of sexual maturity and increase in lifespan • caloric restriction delays sexual maturation & increases lifespan - cause and effect?? or more complicated? Lifespan correlates with length of development to adulthood • period of adult development predicts maximum lifespan * note discrepancy in relative time investment to develop How/why might lifespan be related to sexual development? • all organisms have limited amount of total energy which can be all spent on vital functions spent - initially, most energy for growth growth - always must expend some energy to repair damage due repair to normal metabolism, etc. - also spend energy on defense (both predators & disease) defense - once mature, significant energy spent on reproduction once reproduction * organism must survive for reproduction • but can be a trade-off between reproduction and repair, etc. but - different species may utilize different strategies to maximize fitness to How/why might lifespan be related to sexual development? • theorize that if favor repair, then organism could be very long-lived; conversely, if favor reproduction, then little energy available for repair and shorter lifespan is predicted • humans live long and reproduce little; rodents live a short life but reproduce robustly • salmon = favors repair and maintenance (moves to ocean where grows larger and stronger than it could in fresh water) then drastically shifts strategies devoting all energy to reproduction during its terminal spawn (doesn't eat or repair, just moves upstream & mates) • C. elegans = a mutant lives 2X longer than wild types; all aging features are slowed in the mutant; also has a very low birth rate Age changes in dividing cells • experimentally, how do we begin to address intrinsic versus extrinsic theories of aging on a cellular level? - if remove a cell from the body and allow look at cell division under favorable conditions, will it : 1) divide forever ? (extrinsic theory; environment good) 2) eventually stop dividing ? (intrinsic theory; genetic program tells it to stop) Hayflick effect
• Hayflick: tested the ideas using cultured fibroblasts - skin cells grown in a flask until confluent (stop dividing due to contact inhibition) - collect cells, divide into two flasks and allow them to divide until confluent again - this new cell division represents one population doubling (PD) • experimental result = rate of cell division slowed at ~45 PD rate and stopped at ~60 PD stopped - called the Hayflick Effect or Hayflick Limit - cells are not immortal - this result may be a true aging effect: universal, progressive, senescent, (and irreversible) universal, Hayflick effect
• what if you look at cells from older persons? *observe fewer PD in cells from older donors • what about species differences? Would you expect to observe different PDs in species with short vs. long long lifespans?? * mice, rats (max. lifespan ~ 2-3 yr) show fewer PDs than human (max. lifespan 125 yrs) which shows fewer PDs than Galapagos turtle (max. lifespan 200 yrs) Hayflick effect
• the number of PDs is proportional to the maximum lifespan across species • Hayflick effect is evidence of intrinsic factors in aging on a intrinsic cellular level cellular ...
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This note was uploaded on 01/16/2011 for the course GERO 310 taught by Professor Davies during the Fall '09 term at USC.
- Fall '09