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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
Where is resveratrol found
Red wine
26
Over expression increases longevity in yeast, flies, worms, mice on high fat diet
Sirtuins
27
``` 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 ```
Hallmarks of aging
28
Loss of proteostasis is a
Hallmark of again
29
Progressive cognitive disease with memory loss and other symptoms
Alzheimer's disease
30
Amyloid plaques, Neurofibrillary tangles, and brain shrinkage occur in
Alzheimer's disease
31
A hallmark of aging that relates to how the DNA is packaged
epigenetic alterations
32
If you can change the histones are interacting with DNA you can change how the DNA is working based on whats expressed
epigenetic alterations
33
epigenetic alterations of DNA effect
expression
34
Things that cause normally folded proteins to become miss folded
heat shock, changes in the ER, and oxidative stress
35
Miss folded proteins are degreased by being sucked into a lysosome
Autophagy
36
Miss folded proteins are marked with ubiquitin to be degraded by proteosomes
proteasomal degradation
37
Miss folded proteins can be refolded by
chaperons
38
do most cell stop dividing in later years
yes
39
Amyloid precursor protein
APP
40
fAD is caused by a mutation in
APP
41
The causes if sAD are
not well known
42
over expression on a high fat diet increases longevity
sirtuins
43
DNA repair activity correlates with
longevity
44
Aging hallmark that relates to DNA repair activity
genomic stability
45
Structures at the ends of chromosomes
Telomeres
46
What happens to the lengths of telomeres with age in somatic cells
Shorten
47
Telomere sequence in mammals
TTAGGG
48
F ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3' end of DNA
Telomerase
49
RNA dependent DNA polymerase
Telomerase
50
Two pathways are thought to be involved in dietary restriction way to increase life span
Pathways involving IGF and SIRT1
51
Progerias cause accelerated aging and affect DNA gyrases for repair and nuclear lamin
genetic instability
52
Boosting what could also lead to the release of SIRT1
NAD+
53
early again syndromes involved damage to
helicase
54
why is helicase important for preventing DNA again
allows for DNA repair
55
Tissues has cells that are undifferentiated that can divide to replenish themselves or the cells in tissue
Stem cells
56
An again hallmark that is a result of depletion stem cells
stem cell exhaustion
57
stem cell depletion can lead to
inflammation
58
When cells stop dividing, can be trigged by damaged
cellular senescence
59
Somatic animal cells can divide around 60 times before they are stagnant in a laboratory setting is called
Hayflick limit
60
When the hay flick limit is reached in the body what happens
Senescent cells accumulate
61
What is a problem with cellular senescence
secrete unwanted things
62
What are some of the things senescent cells secrete
growth factor, cytokines
63
Drugs that target senescent cells and has been show to renew organs in mice
senolytic cells
64
what cells are telomerase's found in
germ cells and tumor cells
65
what do telomeres help to prevent?
lose of DNA segments
66
Early aging disease caused by mutations in DNA gyrase (used in repair) or nuclear lamin
progerias
67
in mice research, do antioxidants extend the life?
NO
68
the healthy period of life
health span
69
rather than extending lifespan we should focus on extending
healthspan
70
When people age, diseases increase which decrease the quality of life and burdens society
reasons for healtspan over lifespan
71
in some studies increase oxidation have been show to do what that goes against the free radical theory
increases lifespan

Biochem Exam III (3 decks)

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