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18 Cards in this Set
- Front
- Back
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Evolutionary senescence theory |
Failure of NS to select late-life traits Senescence = deteriorates with age Why do we age? |
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Mutation accumulation theory |
Genes that are detrimental in late life can still be passed out Why do we age? |
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Antagonist pleitropy theory |
Some genes are beneficial early in life are deleterious later in life E.g. p53 gene helps prevent cancer in young people, but plays role in aging by decreasing ability to renew tissues Why do we age? |
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Disposable soma theory |
Hazardous environment favors early reproduction and short life spans E.g. predator-free opossums love much longer and age less than those who love w/ predators Why do we age? |
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Programmed theory of aging |
Biological time table of aging via genetics (unfit eliminated to make room for next) How do we age? |
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Damage / Error theory of aging |
Cumulative damage from environmental assaults How do we age? |
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Cross-linking glycation hypothesis |
Over time, proteins, DNA, and other structural molecules develop inappropriate attachments, which decrease mobility and elasticity (collagen -> skin wrinkling, etc.) E.g. Glu forms cross-linked aggregates |
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Genome maintenance hypothesis of aging |
Mutations in somatic cells will not be passed to germ line. Most will be corrected that don’t accumulate / t. DNA repair decreases with age. Werner’s Syndrome: pre-mature aging due to WRN gene (helicase) -> increase abnormalities |
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Damaging agents |
Water (deprotonation / protonation of proteins) Sunlight (rupture of covalent bonds, formation of thymine diners in DNA, cross-linking of proteins, generation of free radicals) |
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Neuroendocrine hypothesis of aging |
Connections b/t brain, NS, endocrine glands. Increase in BP, impaired sugar metabolism, sleep abnormalities Decrease in IGF-1 delays aging (other hormones similar) |
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Oxidative damage |
Normally cleared by anti-oxidants ~90% produced by mitochondria, when one forms, it -> many more Decreased ability to repair w/ age Often from ETC |
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Rate of living theory |
Oldest theory? Mostly rejected. Finite amount of something: E consumption limits longevity, metabolism correlated w/ life span (-> free radical prdxn? Heart beats?) Caloric restriction (lower calories w/o malnutrition) seems to prolong life in some mammals. |
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Replicative/cellular senescence hypothesis |
Hayflick limit: cells have limited ability to reproduce, likely due to telomere shortening (40-60 replications; RNA priming causes loss of segment of telomere. After ~100 divisions, telomere short enough to senesce (stop dividing). Is this the clock? Probably not—typically lengthened by telomerase, not all tissues have actively dividing cells, shortening is not universal among species, etc. |
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Collagenase in aging |
Released if skin cells senesce, -> thinning of skin? Cancer: young pts may use to decrease replication of damaged cells, in elderly, senescence -> antagonist pleiotropy |
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Age-related changes in body fat / H2O / integumentary |
Fat-free mass (body mass - adipose fat) and lean body mass (fat-free - bone - non-adipose mass) decrease Increased fat around abdominal viscera and abdominal subcutaneous tissue, and decrease facial fat Integ: epidermis thins, keratinocytes proliferate slower, melanocytes decrease (less protection from UV), fewer Langerhan’s (lower immune response). Dermis decreases in elastin / collagen. Slower nail growth, fewer sweat glands. |
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Age-related msk changes and sensory changes |
Msk: Sarcopenia (reduced muscle mass) > 50 yo, fewer and smaller muscle fibers, decreased motor neuron activity and recruiting type 2 motor units. Bones: increase bone resorption:formation -> decrease density Articulate cartilages thin because reduced water Fewer hair cells on organ of Corti (nerve connections) so loss of hearing Fewer cones and less adaptation of pupil and rods, so decreased vision Less active olefaction so decreases taste |
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Age-related motor / cognitive / CV / Pulm changes |
Motor: slower rxn time—reduced central processing Cognitive: not much w/o dementia CV: artherosclerosis risk, but w/o just reduced distension of arteries Pulm: w/o COPD, just reduced type IIa fibers (reduced endurance / strength) |
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Age-related changes in exercise, renal, GI, endo |
Exercise: Renal: GI: Endo: reduces almost all hormones—insulin (-glu tolerance—+adipose), HGH/IGF-1 (-pulsatory actions of somatotrophs), adrenal steroids (no change in cortisol/aldosterone, but dehydroxyandrosterone decreases), thyroid hormone stable til >100, parathyroid hormone increases, gonadal horm. decreases sharply for females at menopause (~50), andropause slower |
