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Pharmacology 200 > 3 - anti-aging > Flashcards

3 - anti-aging Flashcards

(79 cards)

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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
what is the DAF16 receptor in humans
FOXO transcription factor
26
what happens when you have a mutations in the IGF-1 activity
often linked to living loner
27
what happens with FOXO variants (maybe like extra)
linked to longevity
28
what happens in type 2 diabetes
excessive reduction in insulin signalling
29
what is LY924002
ATP competitive drug to reduce the insulin pathway
30
what happens when you use peptides which act as competitive inhibitors of the insulin receptor
lifespan increases because the pathway is reduced
31
what happens when you use peptides which act as activators of the insulin receptor
lifespan decreases because the pathway is increased
32
what is Wortmannin
non competitive inhibitor that inhibits P13K enzyme and blocks the insulin pathway
33
what happens when you knockout SIR2 in yeast
shortens lifespan
34
what happens when you overexpress SIR2 in yeast
extends lifespan
35
what is acetylation and where does it add to (aa)
post-translational modification that is added to lysine residues
36
what does acetylation regulate
protein activity, stability, localization and structure
37
what are some examples of acetylation
histones/chromatin structure
38
what happens to levels of acetylation during aging
levels of acetylation can be deregulated
39
what kind of molecule is SIR2
a nucelar deacetylase enzyme (removes acetylation from proteins)
40
how does SIR2 do its enzyme stuff (what does it use)
it uses NAD as a cofactor
41
what is NAD+
metabolic intermediate which has roles in glycolysis and CAC
42
what happens to NAD+ levels when energy is low
NAD+ is high
43
what does CR do to SIR2 and how
activate by raising NAD+ which activates SIRT1
44
what happens to NAD+ levels when energy is high (after eating)
low because NADH is formed
45
what is SIRT2=? in mammals
SIRT1
46
what are 2 main things that SIRT1 does
improves lifespan and healthspan (healthy years of one's life)
47
what binds in the SIRT 1 active site
NAD
48
what is resveratrol
an allosteric sir2/ sirt1 activator
49
what is SRT1720
an allosteric sir2/ sirt1 activator
50
what can resveratrol and SRT1720 do
protect against heart disease, cancers, diaBETES, ALzHEiMERS
51
STR1720
bioactivity :D
52
how does boosting NAD+ affect SIRT1
it can activate SIRT1 because there are more co-substrates to activate it
53
why cant we just take NAD+ pills to live forever
because it is large and charged and cant really permeate into the cell
54
what drugs can we use to boost NAD+ in the body
NR and NMN precursors
55
what do you do to mTOR if you want to increase lifespan
inhibit
56
what happens to mTOR during CR
it is suppressed
57
which pathway is mTOR linked to
lots of other longevity pathways
58
what kind of molecule is mTOR
a serine/threonine protein kinase of the PI3K-related family
59
what does mTOR do
regulates cell growth and metabolism in response to nutrients and hormones (adds phosphorylation post-translational)
60
what does rapamycin do
inhibits mTOR through the formation of a bridged ternary complex
61
what is a way that you can use rapamycin
immunosuppressant or cancer drug
62
how can you change the AAK-2 pathway to extend lifespan
overexpress it
63
what happens to AAK-2 during CR
activated
64
which two pathways do you want to increase to increase life span
AAK-2/AMPK and SIRT1/2
65
which two pathways do you want to decrease to increase life span
insulin/IGF-1 & DAF-2 | mTOR
66
what other pathways is AAK-2 involved in
many other pathways involved in aging
67
what is AAK-2 in mammals
AMPK
68
what does AMPK do
adds phosphorylation to proteins (post translational modifications)
69
what happens to AMPK with low nutrient levels and why
activated because AMP is high
70
what happens to AMPK with high nutrient levels
not activated because AMP is low
71
what does AMPK need to be activated
AMP
72
what does AMPK do to insulin sensitivity
increases is
73
what does AMPK do to sirtuins and mTOR
AMPK activates sirtuins and represses mTOR
74
what does metformin do and how
activates AMPK indirectly (probably through ETC complex 1)
75
why is metformin used for insulin
because it is insulin sensitizing
76
what does AICAR do
mimics AMP to be a direct activator of AMPK
77
is AICAR permeable
not permeable
78
resveratrol is an allosteric activator of which enzyme
SIRT1
79
what is the difference with crRNA, gRNA and sgRNA
they all the same for our info, all CRISPR RNA

Pharmacology 200 (29 decks)

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