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Biochem Exam III > Aging SG > Flashcards

Aging SG Flashcards

1
Q

Degrade miss folded proteins

A

lysosomes and proteasome

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2
Q

Used as a marker for proteasomal degradation

A

ubiquitin

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3
Q

aggregation of miss folded proteins is a sing of

A

aging

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4
Q

Family of NAD+ dependent deacetylase proteins

A

Sirtuins

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5
Q

Related to SIR2 (Silent information regulator) in yeast

A

Sirtuins

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6
Q

What are the two types of Alzheimer’s disease

A

sAD and fAD

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7
Q

What type of Alzheimer’s disease is the most common?

A

sAD

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8
Q

What type of Alzheimer’s disease is early onset

A

fAD

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9
Q

What type of Alzheimer’s disease is rare

A

fAD

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10
Q

What type of Alzheimer’s disease is late onset (<65)

A

sAD

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11
Q

Alzheimer’s disease is though to be caused (at least in part) by

A

miss folded proteins

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12
Q

What results in an accumulation of miss folded proteins

A

loss of proteostasis

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13
Q

A loss of proteostasis can lead to

A

Alzheimer’s disease

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14
Q

What allele is related to sAD

A

Apolipoprotein E (APOE4 allele)

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15
Q

Two proteins that when mutated are involved with fAD

A

Amyloid precursor protein (APP)

Presenilin 1 & 2

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16
Q

Presenilin 1 & 2 is involved with what protein

A

gamma secretase

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17
Q

While in fAD gamma secretase is the protien with a mutation, what also has t0 be present in order for there to be plaque accumulation (alpha or beta secretase)

A

beta

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18
Q

Genetic diseases with premature aging

A

progeroid syndrome

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19
Q

DNA repair activity correlates with

A

longevity

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20
Q

DNA repair activity is related to which hallmark of again

A

Genetic instability

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21
Q

Syndromes caused by mutations in DNA helicases involved in repair

A

Werner’s and Bloom’s syndromes

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22
Q

Syndromes caused by mutation in prelamin A

A

Hutchinson-Gilford syndrome

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23
Q

Hutchinson-Gilford, Werner’s, and Bloom’s syndromes are all related to

A

premature again

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24
Q

Binds to SIRT1 and activates deacetylase

A

Resveratrol

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25
Q

Where is resveratrol found

A

Red wine

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26
Q

Over expression increases longevity in yeast, flies, worms, mice on high fat diet

A

Sirtuins

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27
Q 
o	Genomic instability
o	Telomere attrition
o	Epigenetic alterations
o	Loss of proteostasis
o	Deregulated nutrient sensing
o	Mitochondrial dysfunction
o	Cellular senescence
o	Stem cell exhaustion
o	Altered intracellular communication
A

Hallmarks of aging

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28
Q

Loss of proteostasis is a

A

Hallmark of again

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29
Q

Progressive cognitive disease with memory loss and other symptoms

A

Alzheimer’s disease

30
Q

Amyloid plaques, Neurofibrillary tangles, and brain shrinkage occur in

A

Alzheimer’s disease

31
Q

A hallmark of aging that relates to how the DNA is packaged

A

epigenetic alterations

32
Q

If you can change the histones are interacting with DNA you can change how the DNA is working based on whats expressed

A

epigenetic alterations

33
Q

epigenetic alterations of DNA effect

A

expression

34
Q

Things that cause normally folded proteins to become miss folded

A

heat shock, changes in the ER, and oxidative stress

35
Q

Miss folded proteins are degreased by being sucked into a lysosome

A

Autophagy

36
Q

Miss folded proteins are marked with ubiquitin to be degraded by proteosomes

A

proteasomal degradation

37
Q

Miss folded proteins can be refolded by

A

chaperons

38
Q

do most cell stop dividing in later years

A

yes

39
Q

Amyloid precursor protein

A

APP

40
Q

fAD is caused by a mutation in

A

APP

41
Q

The causes if sAD are

A

not well known

42
Q

over expression on a high fat diet increases longevity

A

sirtuins

43
Q

DNA repair activity correlates with

A

longevity

44
Q

Aging hallmark that relates to DNA repair activity

A

genomic stability

45
Q

Structures at the ends of chromosomes

A

Telomeres

46
Q

What happens to the lengths of telomeres with age in somatic cells

A

Shorten

47
Q

Telomere sequence in mammals

A

TTAGGG

48
Q

F ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3’ end of DNA

A

Telomerase

49
Q

RNA dependent DNA polymerase

A

Telomerase

50
Q

Two pathways are thought to be involved in dietary restriction way to increase life span

A

Pathways involving IGF and SIRT1

51
Q

Progerias cause accelerated aging and affect DNA gyrases for repair and nuclear lamin

A

genetic instability

52
Q

Boosting what could also lead to the release of SIRT1

A

NAD+

53
Q

early again syndromes involved damage to

A

helicase

54
Q

why is helicase important for preventing DNA again

A

allows for DNA repair

55
Q

Tissues has cells that are undifferentiated that can divide to replenish themselves or the cells in tissue

A

Stem cells

56
Q

An again hallmark that is a result of depletion stem cells

A

stem cell exhaustion

57
Q

stem cell depletion can lead to

A

inflammation

58
Q

When cells stop dividing, can be trigged by damaged

A

cellular senescence

59
Q

Somatic animal cells can divide around 60 times before they are stagnant in a laboratory setting is called

A

Hayflick limit

60
Q

When the hay flick limit is reached in the body what happens

A

Senescent cells accumulate

61
Q

What is a problem with cellular senescence

A

secrete unwanted things

62
Q

What are some of the things senescent cells secrete

A

growth factor, cytokines

63
Q

Drugs that target senescent cells and has been show to renew organs in mice

A

senolytic cells

64
Q

what cells are telomerase’s found in

A

germ cells and tumor cells

65
Q

what do telomeres help to prevent?

A

lose of DNA segments

66
Q

Early aging disease caused by mutations in DNA gyrase (used in repair) or nuclear lamin

A

progerias

67
Q

in mice research, do antioxidants extend the life?

A

NO

68
Q

the healthy period of life

A

health span

69
Q

rather than extending lifespan we should focus on extending

A

healthspan

70
Q

When people age, diseases increase which decrease the quality of life and burdens society

A

reasons for healtspan over lifespan

71
Q

in some studies increase oxidation have been show to do what that goes against the free radical theory

A

increases lifespan

Biochem Exam III (3 decks)

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