MCP 11

Question 0

emerging theory on aging

Answer 0

aging results from a decline in the force of natural selection on traits acting in late life.

Question 1

gompertz law of human mortality

Answer 1

the death rate increases exponentially with age in a protected environment where external causes of death become negligible. after age of 25ish, your chance of death doubles every 8 years

Question 2

mutation accumulation theory of aging

Answer 2

the force of selection is too weak to oppose the accumulation of germ line mutations with late acting deleterious effects. late onset of certain diseases allows people who have genes for them to reproduce

Question 3

antagonistic pleiotropy theory of aging

Answer 3

some genes may be selected for beneficial effects on reproductive and survival successes early in life, but the same genes have unselected deleterious effects with age, which contributes to aging. aging is a trade off of reproductive and survival success

Question 4

disposal soma theory of aging

Answer 4

evolution acts primarily to maximize reproductive fitness. the soma (non-reproductive aspects of the organism) is maintained only for reproductive success and becomes disposable after reproductive success. aging is the result of natural accumulation of damage to the soma

Question 5

benefits of studying aging

Answer 5

increasing healthspan and treating early onset degenerative diseases. compression of morbidity, or delaying onset of aging related degenerative disorders. it is thought that aging and aging related degenerative diseases (parkinsons, etc) are linked

Question 6

cellular and molecular hallmarks of aging

Answer 6

genome instability, telomere attrition, epigenetic alterations, proteostatic stres, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication

Question 7

free radical (oxidative stress) theory of aging

Answer 7

toxic byproducts of metabolism can damage cellular components and lead to aging. reactive oxygen species in particular. mitochondrial damage results in increased ROS production, leading to a vicious cycle. studies show, however, that oxidative stress is not the driving force of aging in mice

Question 8

mitochondrial theory of aging

Answer 8

mitochondrial damage during aging, manifested by mutations or deletions in mitochondrial DNA, oxidation, structural destabilization, changes in membrane lipid composition, and alterations for mitochondrial dynamics and quality control. contributes to aging by reduced energy production, increased cell death, defective iron-sulfur biosynthesis leading to genome instability, altered redox balance and ROS signaling, and affecting global protein homeostasis

Question 9

cell senescence/telomere theory of aging

Answer 9

DNA damage was found to trigger senescence, or permanent arrest of cell division. telomere erosion is a DNA damage that leads to this. when telomeres get too short, they cause a double strand break and stop reproduction of that cell. studies have shone that telomere length and lifespan is poorly conserved. mice have long telomeres but short lives

Question 10

somatic mutation theory of aging

Answer 10

unrepaired DNA adducts may accumulate to interfere with transcription, leading to death of cell

Question 11

proteostatic stress theory of aging

Answer 11

stress induced by loss of protein homeostasis. leads to protein dysfunction, cell membrane disruptuon, and formation of toxic protein aggregates, and cell death. error catastrophe theory of aging predicts that aging is due to increased errors in protein synthesis

Question 12

animal models of extended lifespan

Answer 12

Ames and Snell mice. mutations that reduce GH and IGF-1. grow to a third of the size of their siblings but live way longer. less susceptible to cancer and have lower blood insulin. delaying aging can suppress diabetes and cancer.

Question 13

insulin and IGF-1 signaling pathway (IIS) effects on aging

Answer 13

downstream effectors that include the FOXO and mTOR families. increased FOXO and decreased mTOR promote longevity. FOXO promote a bunch of different genes, and protect undamaged cells in energy utilizing tissues. mTOR are kinases that respond to stress, nutrients and growth factors.

Question 14

FOXO3A

Answer 14

associated with longevity. component of signaling pathways that control growth, metabolism, and stress resistance

Question 15

CETP

Answer 15

associated with longevity. plasma protein that facilitates transport of cholestrol esters and triglycerides between lipoproteins

Question 16

APOC3

Answer 16

component of VLDL that inhibits lipoprotein lipase and hepatic uptake of triglyceride rich particles

Question 17

TOMM40

Answer 17

encodes protein translocase on the mitochondrial outer membrane, suggesting that variations in mitochondrial function may contribute to differences in longevity

Question 18

segmental progeroid syndromes

Answer 18

diseases that exhibit premature aging phenotypes in a subset of tissue or organ systems. hutchinson gilford progeria syndrome is an example

Question 19

caloric/dietary restriction as a means to counter aging

Answer 19

restriction of calories without undernutrition would retard aging and prolong lifespan of rats. how it works: activation of FOXO transcriptional factor. Reduced mTOR signaling. activation of the adenosine monophosphate (AMP) activated protein kinase (AMPK). increased autophagy

Question 20

exercise as a way of preventing aging

Answer 20

excercise increases ATP synth and O2 consumption. This increases the hormone response and stress signalling. This increases mitochondrial density, metabolic capacity, and resistance to oxidative stress. This leads to an increased bioenergetic reserve. muscle use prevents sarcopenia, or loss of muscle mass and function.

Question 21

pill to prevent aging

Answer 21

have a pill that reduces mTOR (rapamycin)

not sure what the effects are