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PHS 931 > Block 3 Lecture 2 -- Cell Death > Flashcards

Block 3 Lecture 2 -- Cell Death Flashcards

1
Q

What are the 2 categories of aging theories?

A

1) biologically programmed

2) Accumulation of Errors / Damage

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2
Q

What is the programmed senescence theory?

A

genetics regulate program

    • Hayflicks limits
    • Telomerase theory
    • based on salmon spawning producing massing steroid release leading to death
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3
Q

What is Hayflicks limits?

A

fibroblasts die after 50 divisions

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4
Q

What are the biologically programmed theories?

A

1) programmed senescence
2) immune senescence
3) endocrine senescence

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5
Q

What is the endocrine senescence theory?

A

decreased HP-ovarian fx leads to sexual senescence and hormone decreases, along with less responsive organs
– more difficult to maintain homeostasis

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6
Q

What is the immune senescence theory?

A

change in immune system leads to infection disease

    • fewer Th
    • thymic involution
    • more autoimmune diseases
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7
Q

What is the Rate of Living Theory?

A

greater basal O2 metabolism = shorter lifespan

– supported by caloric restriction studies

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8
Q

What is the Failure of Neurogenesis theory?

A

based on finding that neurogenesis required throughout life in some parts of brain

    • hippocampus
    • olfactory bulb
    • crucial for synaptic plasticity (learning, memory)
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9
Q

What theory of aging has the best evidence?

A

free radical theory

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10
Q

What are the Damage theories?

A

1) free radical
2) failure of endogenous repair
3) failure of neurogenesis
4) environmental exposures
5) rate of living
6) wear and tear

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11
Q

What is the failure of endogenous repair mechanisms theory?

A

environmental exposures neutralized by neurotrophins, DNA repair, etc.

    • neurotrophins turned off during CNS development
    • turned on after trauma/toxicity
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12
Q

What is the free radical theory?

A

slow persistent accumulating DNA/protein/lipid damage

– mitochondrial death switch

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13
Q

What is nuclear compaction?

A

process that occurs in apoptosis

    • chromatin condensation
    • DNA cleavage
    • formation of apoptotic bodies
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14
Q

Why is apoptosis better?

A

plasma membrane stays intact

– minimal inflammatory response

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15
Q

What substances induce necrosis?

A

trauma, toxins, hypoxia
Ca overload, oxidative stress
– cellular swelling causes rupture of all membranes

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16
Q

What causes secondary brain damage?

A

microglia scavenging remainders of cell death

– apoptosis and necrosis

17
Q

What defends against ROS?

A

enzymes
– SOD, GSH peroxidase, catalase
antioxidants
– GSH, polyphenols, Vit. E + C

18
Q

Why are neurons especially vulnerable to ROS?

A

1) high demand
- - many cells, long axons
2) little capacity to make/store energy
3) metabolic demands increase with age

19
Q

SOD:

A

O2. (superoxide) – H2O2

20
Q

Fe catalyzes:

A

H2O2 – OH. (hydroxyl radical)

the fenton reaction

21
Q

GSH Peroxidase catalyzes:

A

H2O2 – H2O

22
Q

Catalase catalyzes:

A

H2O2 – H2O + O2

23
Q

What disease has an SOD mutation?

A

ALS

24
Q

O2. + NO. (from Arg) –

A

ONOO- (peroxynitrite)

25
Q

What substances mediate cellular damage due to ROS?

A

OH. (Hydroxyl radical)

ONOO- (peroxynitrite)

26
Q

Where does iron accumulate?

A

nigrostriatal pathway (PD)

27
Q

Why is ATP required to prevent excitotoxicity?

A

EAATs require ATP

28
Q

When does Glu (Ca Overload) Excitotoxicity occur and what is the overall result?

A

after ischemia or TBI

    • delayed inflammation
    • prolonged apoptosis
29
Q

Why is Ca overload bad?

A

1) enzyme (-ase) activation
2) NOS makes NO
NO + AA = OH. (ROS)

30
Q

What are the Ca-buffering systems?

A

1) ATP-dependent Ca uptake pumps (ER, mito)
2) cytosolic Ca sensors (calmodulin)
3) cytosolic Ca binding proteins (calbindin)

31
Q

What are the phases of excitotoxicity in stroke?

A

1) Glu causes NMDAr agonism, Ca influx
2) increased ACh agonises a7 nAChR, Ca influx
3) can’t buffer Ca (no ATP)

32
Q

Injury produces…

A

inhibitory growth molecules (spinal cord won’t heal!)

33
Q

MoA of memantine:

A

NMDAr antagonist

    • no neuroprotective evidence, although PCP and ketamine do work for this
    • no cognitive dysfunction as in PCP/ketamine
    • decrease Ca influx (?)
34
Q

What pharmacological agents can be used for neuroprotection?

A

1) NMDAr antagonist
2) a7 nAChR antagonists
3) CCBs
4) anti-oxidants
5) COX-1 NSAIDs
6) neurotrophic factors

35
Q

What algae is a big DHA producer?

A

crypthecodinium cohnii

36
Q

DHA treatment has what effect on brain inflammation after TBI?

A

reduces, mainly in post-injury administration

37
Q

What is the MOA of w-3 FAs?

A

antioxidant

GPCR modulator

PHS 931 (29 decks)

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