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Neorologia > Cell Death > Flashcards

Cell Death Flashcards

1
Q

Biological Programmed Theories of Aging

A
  • Programmed Senescence Theory
  • Endocrine senescence theory
  • Immune Senescence theory
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2
Q

Accumulation of Errors or Damage Theories of Aging

A
  • Wear and Tear
  • Rate-of-living
  • Environmental Exposures Theory
  • Failure to repair and neurogenesis
  • Free Radical
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3
Q

Programmed Genetic Senescence Theory

A
  • Genes regulate a “program” of bodily aging
  • after spawning - massive corticosteroid release leading to death of salmon
  • “hayflick’s limits”
  • Telomerase Theory of Aging
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4
Q

Endocrine homeostasis theory

A
  • Decreased hypothalamic/pit/ovarian function leading to sexual senscence
  • Decrease in additional hormones (GH, melatonin)
  • Difficult to maintain homeostasis as we age
    1) decline in production of hormones
    2) Target organs respond less
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5
Q

Immune Homeostasis Theory

A

Changes in the immune system lead to increased infections and disease vulnerability.

  • Decrease in T helper cells
  • Increase in autoimmune diseases
  • Involution of Thymus
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6
Q

Accumulation of Damage and Errors

A

Cellular function –> Oxygen/glucose use –> accumulating cell debris

  • Live fast die young
  • Failure of one system causes failure of all
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7
Q

Rate of Living Theory

A
  • All cells have a metabolic “bank account”
  • Once consumed allotment of calories, systems fail
  • Greater oxygen basal metabolism, shorter lifespan
  • Caloric restriction studies
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8
Q

Failure of neurogenesis theory

A

Neurogenesis occurs throughout life in the:

1) Hippocampus
2) Olfactory bulb

-Crucial for synaptic plasticity and learning

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9
Q

Failure of endogenous repair mechanisms

A
  • Exogenous exposure to toxins

- Failure of neurotrophic signalling to be turned back on –> failure to repair

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10
Q

Oxidative stress/Free Radical theory

A
  • Free radicals causing damage
  • Slow accumulation o fdamage
  • Mitochondria acting as death switch for neurons
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11
Q

Appropriate Cell Death

A

-Apoptosis
-Part of normal brain development
Induced by neurotrophic factor withdrawal
-Multiple genes coordinate

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12
Q

Inappropriate Cell Death

A

-Apoptotic (active)
-Necrotic (passive)
-
Apoptosis following mild cellular stressor
-Necrotic cells placed in toxic environments and passively die (low O2, high temp, trauma, toxicants, disease)

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13
Q

Apoptosis: Intrinsic vs. Extrinsic

A
  • Intrinsic: mitochondrial impairment: BAX/bad insertion and release of procaspase 9
  • Extrinsic: Death signal binding: Procaspase 8
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14
Q

Apoptosis Process

A
  • Nuclear Compaction
  • Chromatin condensation
  • DNA cleavage
  • Blebbing
  • Formation of apoptotic bodies
  • Microglia scavenge what is left
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15
Q

How is it that cellular constituents do not cause inflammatory response after apoptosis

A

Plasma membrane stays intact, not released into the local environment

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16
Q

Necrosis Process

A
  • Cellular swelling is followed by rupture of all cell membranes
  • All constituents are dumped into local area causing secondary damage
  • Associated with robust inflammation and microglial inflammation
17
Q

ROS and CNS DAmage

A

Metabolism of oxygen and Ca++ overload can lead to damage in neurons

18
Q

What are endogenous and exogenous causes for Ox Stress

A
  • Endogenous: Mitochondria, Peroxisomes, Inflammatory cell

- Exogenous: Radiation, Ozone, Xenobiotics

19
Q

Defense System for ROS

Enzymatic and non enzymatic

A

Enzymatic: Superoxide dismutase, Glutathione peroxidase, Catalase

Non-enzymatic: Vitemin E, C, Glutathione, Polyphenols

20
Q

Why are Neurons particularily vulnerable to ROS?

A

1) High metabolic demand
2) little capacity to make or store energy
3) metabolic demands increase with age

21
Q

Why do ROS beget ROS

A

If Glucose/ox availibility is reduced, cannot make ATP and calcium buffering /glutamate reuptake are reduced

22
Q

Specific effects of ROS

A
  • DNA strand breaks
  • Protein Nitration
  • Lipid peroxidation
  • Iron catalyst increases speed
23
Q

What is the most studied excitotoxicity?

Why

A

Calcium Overload
Huge neuron death on the order of a few minutes
Ischemiia or trauma

24
Q

Three Proteins involved in calcium buffering

A

1) ATP-dependent CA pump: mitochondria and ER
2) Cytosolic Ca sensor: Calmodulin
3) Cytosolic Ca binding proteins: Calbindin`

25
Q

How does ischemic stroke cause excito toxicity

A 
Lack of oxygen and Glc
No ATP
Ca++ and GLU buffering fails
Calcium overload
Uncontrolled neurotransmitter release
Ca Dependent lipases, DNAases, proteases

Neorologia (12 decks)

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