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L2 Stem Cells > Ageing and senescence > Flashcards

Ageing and senescence Flashcards

1
Q

What is senescence?

A

An age related decline in function

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2
Q

What is the disposable soma theory?

A

As soon as an individual can’t increase the number/chance of survival of its offspring any further there is no natural selection against decline in that individual

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3
Q

What is a senescence factor?

A

Something that drives ageing

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4
Q

What are the major senescence factors? (3)

A
  • Metabolism
  • Reactive oxygen species (ROS)
  • DNA damage (Progeria syndromes)
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5
Q

What are the major factors that increase lifespan? (3)

A
  • Dietary restriction
  • Environmental stresses
  • Signals from the somatic gonad
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6
Q

What is the rate of living theory? (2)

A
  • Animals with a high metabolism have a shorter lifespan
  • Large animals live longer, cold blooded animals live longer at lower temperatures
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7
Q

What is the ROS theory of ageing?

A

Oxygen molecules with an unpaired electron cause oxidative damage which causes ageing

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8
Q

What happens if you give an animal more ROS?

A

Increases lifespan - goes against the theory

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9
Q

What do longevity genes do?

A

Induce resistance to oxidative stress

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10
Q

What is the DNA damage theory of ageing? (2)

A
  • Unrepaired/unrepairable DNA may accumulate in non-replicating cells and cause ageing (not higher mutation rate)
  • NAD depletion via excessive PARP activation could result in senescent cells
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11
Q

What is the role of PARP?

A

PARP is an enzyme that responds to DNA damage and requires co-factor NAD

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12
Q

What is a senescent cell?

A

A cell which is aged no longer divides but isn’t dead (zombie cell)

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13
Q

How might senescent cells drive ageing? (2)

A
  • Could be hogging the stem cell niches and getting in the way
  • Secretion of SASP factors
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14
Q

What are the actions of SASP secretions? (3)

A
  • Pro-inflammatory
  • Cause tissue remodelling
  • Induce senescence in neighbouring cells
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15
Q

How does dietary restriction affect lifespan?

A

Appears to increase lifespan

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16
Q

How do environmental stresses affect lifespan? (2)

A
  • Stresses e.g. heat, ROS generators appear to increase lifespan
  • Hormesis
17
Q

What is hormesis?

A

Low level stresses activate protective mechanisms

18
Q

How might ROS levels increase lifespan? (3)

A
  • Low ROS levels are fine
  • An increase above normal allows activation of protective mechanisms
  • Taking high levels of antioxidants would negatively interfere with this system
19
Q

Which pathways are involved in ageing? (3)

A
  • IGF
  • TOR
  • Sirtuins
20
Q

How is the IGF pathway involved in ageing?

A

Blocking IGF increases lifespan

21
Q

How is the TOR pathway involved in ageing?

A

Blocking TOR increases lifespan

22
Q

How is the Sirtuins pathway involved in ageing?

A

Overexpression of Sirtuins increases lifespan

23
Q

What happens to C.elegans if you block IGF signalling?

A

Enters dauer stage and lives longer

24
Q

What does the IGF pathway do?

A

Blocks the nuclear localisation of DAF16/FOXO

25
Q

What is the mammalian version of DAF16?

A

FOXO

26
Q

What is DAF16/FOXO?

A

A transcription factor that enters the nucleus and promotes anti-ageing functions

27
Q

How does dietary restriction increase lifespan?

A

Blocks the IGF pathway

28
Q

What genes does DAF16/FOXO activate? (4)

A
  • Antioxidant genes
  • Metabolic genes
  • Chaperone genes
  • Antibacterial genes
29
Q

What does TOR signalling do?

A

TOR kinase is a nutrient sensor that stimulates growth and blocks repair pathways e.g. autophagy when food is plentiful

30
Q

What is the TOR pathway? (3)

A
  • TOR activates S6K1 and inhibits 4E-BP1
  • S6K1 stimulates growth, 4E-BP1 inhibits growth and activates autophagy
  • TOR is blocked by TSC1-TSC2 kinases which are activated by stress and blocked by growth factors and amino acids
31
Q

How is IGF linked to TOR signalling?

A

IGF is one of the growth factors that blocks TSC1-TSC2, therefore activating TOR

32
Q

What is the effect of rapamycin on lifespan?

A

Blocks TOR kinase and extends lifespan

33
Q

How can the TOR pathway be manipulated to extend lifespan? (3)

A
  • Block S6K1
  • Overexpress 4E-BP1
  • Block TOR
34
Q

What are the Sirtuins?

A

NAD+ dependent protein deacetylases

35
Q

How do the Sirtuins increase lifespan? (2)

A
  • Activates FOXO/DAF16 and UPR-mt response, requires NAD as a cofactor
  • May downregulate IGF pathway
36
Q

What is the UPR-mt response? (2)

A
  • Mitochondrial unfolded protein response
  • Mitochondrial stress response which is linked to longevity
37
Q

What is the NAD depletion theory of ageing? (2)

A
  • NAD levels decline with age
  • Unrepaired DNA damage causes NAD depletion via excessive PARP activation
38
Q

How do signals from the somatic gonad affect lifespan? (2)

A
  • Removal of the germ cells extends lifespan
  • Steroidal hormones dafachronic acid and DAF12 act on DAF16/FOXO in an unknown manner

L2 Stem Cells (12 decks)

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