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Pharmacology 200 > 3 - anti-aging > Flashcards

3 - anti-aging Flashcards

1
Q

what is epigenome

A

compounds that attach to DNA and modify its function, like histone and methylation

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2
Q

what are telomeres

A

small repeated DNA at the end of chromosomes

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3
Q

what is chromosome attrition

A

telomeres are being fully copied, they shorted

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4
Q

what is senescence

A

when cells stop dividing (all cells can only divide a certain amount of times)

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5
Q

what is proteostasis

A

the synthesis and destruction of proteins

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6
Q

what can be an issue with altered proteostasis

A

when there is a buildup of defective proteins

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7
Q

what can be an issue with mitochondrial dysfunction

A

reactive oxidatice damage

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8
Q

what are 5 things that can contribute to biomolecular damage

A
  • genome/epigenome instability
  • telomere attrition
  • mitochondrial dysfunction
  • senescence/stem cell exhaustion
  • altered proteostasis, cell communication and nutrient signalling
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9
Q

what is caloric restriction

A

30% reduction in caloric intake without malnutrition

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10
Q

what is hormesis

A

the body’s stress respsonse

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11
Q

how does CR make less reactive oxygen species (ROS)

A

less food intake which produces less ROS (byproduct of metabolism)

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12
Q

what are 4 possibilities of mechanisms of how CR works

A
  • hormesis
  • less DNA damage
  • less ROS
  • lower metabolism/temp
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13
Q

how were genes involved in longevity identified in the early days

A

random mutagenic screen in genetically tractable organisms with short lifespans (cause DNA damage, breed, see how long they live, see which genes are affected)

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14
Q

how were genes involved in longevity identified currently

A

systemic-wide screen and genome-wide association students

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15
Q

what is systemic-wide screen and genome-wide association students

A

sequences genes of people that live a long life and compare it to people that live a normal life

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16
Q

what is a dauer

A

the vegetative state a worm does into when it is stressed. exists when nutrients and stuff

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17
Q

what was the first longevity gene characterized

A

DAF-2 (Dauer formation-2)

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18
Q

what happens to DAF-16 when you increase DAF-2

A

DAF-16 decreases

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19
Q

what happens when you knockout DAF02

A

worms live twice as long

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20
Q

do you want to increase DAF2 or DAF16

A

DAF16

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21
Q

what happens to the DAF-2 pathway during calorie restriction

A

the pathway is decreased

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22
Q

what is DAF16

A

a downstream transcription factor of DAF2

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23
Q

what happens when you decrease DAF16

A

live shorter

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24
Q

what is the DAF2 receptor in humans

A

insulin/IGF receptor

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25
Q

what is the DAF16 receptor in humans

A

FOXO transcription factor

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26
Q

what happens when you have a mutations in the IGF-1 activity

A

often linked to living loner

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27
Q

what happens with FOXO variants (maybe like extra)

A

linked to longevity

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28
Q

what happens in type 2 diabetes

A

excessive reduction in insulin signalling

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29
Q

what is LY924002

A

ATP competitive drug to reduce the insulin pathway

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30
Q

what happens when you use peptides which act as competitive inhibitors of the insulin receptor

A

lifespan increases because the pathway is reduced

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31
Q

what happens when you use peptides which act as activators of the insulin receptor

A

lifespan decreases because the pathway is increased

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32
Q

what is Wortmannin

A

non competitive inhibitor that inhibits P13K enzyme and blocks the insulin pathway

33
Q

what happens when you knockout SIR2 in yeast

A

shortens lifespan

34
Q

what happens when you overexpress SIR2 in yeast

A

extends lifespan

35
Q

what is acetylation and where does it add to (aa)

A

post-translational modification that is added to lysine residues

36
Q

what does acetylation regulate

A

protein activity, stability, localization and structure

37
Q

what are some examples of acetylation

A

histones/chromatin structure

38
Q

what happens to levels of acetylation during aging

A

levels of acetylation can be deregulated

39
Q

what kind of molecule is SIR2

A

a nucelar deacetylase enzyme (removes acetylation from proteins)

40
Q

how does SIR2 do its enzyme stuff (what does it use)

A

it uses NAD as a cofactor

41
Q

what is NAD+

A

metabolic intermediate which has roles in glycolysis and CAC

42
Q

what happens to NAD+ levels when energy is low

A

NAD+ is high

43
Q

what does CR do to SIR2 and how

A

activate by raising NAD+ which activates SIRT1

44
Q

what happens to NAD+ levels when energy is high (after eating)

A

low because NADH is formed

45
Q

what is SIRT2=? in mammals

46
Q

what are 2 main things that SIRT1 does

A

improves lifespan and healthspan (healthy years of one’s life)

47
Q

what binds in the SIRT 1 active site

48
Q

what is resveratrol

A

an allosteric sir2/ sirt1 activator

49
Q

what is SRT1720

A

an allosteric sir2/ sirt1 activator

50
Q

what can resveratrol and SRT1720 do

A

protect against heart disease, cancers, diaBETES, ALzHEiMERS

51
Q

STR1720

A

bioactivity :D

52
Q

how does boosting NAD+ affect SIRT1

A

it can activate SIRT1 because there are more co-substrates to activate it

53
Q

why cant we just take NAD+ pills to live forever

A

because it is large and charged and cant really permeate into the cell

54
Q

what drugs can we use to boost NAD+ in the body

A

NR and NMN precursors

55
Q

what do you do to mTOR if you want to increase lifespan

56
Q

what happens to mTOR during CR

A

it is suppressed

57
Q

which pathway is mTOR linked to

A

lots of other longevity pathways

58
Q

what kind of molecule is mTOR

A

a serine/threonine protein kinase of the PI3K-related family

59
Q

what does mTOR do

A

regulates cell growth and metabolism in response to nutrients and hormones (adds phosphorylation post-translational)

60
Q

what does rapamycin do

A

inhibits mTOR through the formation of a bridged ternary complex

61
Q

what is a way that you can use rapamycin

A

immunosuppressant or cancer drug

62
Q

how can you change the AAK-2 pathway to extend lifespan

A

overexpress it

63
Q

what happens to AAK-2 during CR

64
Q

which two pathways do you want to increase to increase life span

A

AAK-2/AMPK and SIRT1/2

65
Q

which two pathways do you want to decrease to increase life span

A

insulin/IGF-1 & DAF-2

mTOR

66
Q

what other pathways is AAK-2 involved in

A

many other pathways involved in aging

67
Q

what is AAK-2 in mammals

68
Q

what does AMPK do

A

adds phosphorylation to proteins (post translational modifications)

69
Q

what happens to AMPK with low nutrient levels and why

A

activated because AMP is high

70
Q

what happens to AMPK with high nutrient levels

A

not activated because AMP is low

71
Q

what does AMPK need to be activated

72
Q

what does AMPK do to insulin sensitivity

A

increases is

73
Q

what does AMPK do to sirtuins and mTOR

A

AMPK activates sirtuins and represses mTOR

74
Q

what does metformin do and how

A

activates AMPK indirectly (probably through ETC complex 1)

75
Q

why is metformin used for insulin

A

because it is insulin sensitizing

76
Q

what does AICAR do

A

mimics AMP to be a direct activator of AMPK

77
Q

is AICAR permeable

A

not permeable

78
Q

resveratrol is an allosteric activator of which enzyme

79
Q

what is the difference with crRNA, gRNA and sgRNA

A

they all the same for our info, all CRISPR RNA

Pharmacology 200 (29 decks)

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