Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

17 Cards in this Set

  • Front
  • Back
Describe necrosis.
1. Passive
2. Rupture of the plasma memebrane is the main distinction of necrotic cell death
What happens during apoptosis?
1. Cleavage of DNA into 200bp fragments
2. Cytoplasmic shrinkage and nuclear condensation
3. Cleavage of essential proteins via caspases
What happens to dead cells in apoptosis?
They are packaged into apoptotic bodies and phagocytosed
Is there inflammation around an apoptotic body?
Is apoptosis passive?
No it is ATP dependent
Describe extrinsic mediated apoptosis.
1. Ligand binds to FAS receptor
2. Trimerization of FAS receptor
3. Recruitment of FAD internally
4. Recruitment of caspase 8
5. Caspace 8 recruits and activates caspase 3
6. Caspace 3 induces cleavage associated with apoptosis
Describe intrinsically mediated apoptosis.
1. Some sort of stress causes the ratio of Bax (pro-apop) to Bcl-2 (anti) to shift in favor of BAX
2. This causes the releasal of Cytochrome C from the mitochondria
3. Cytochrom C, Caspase 9, Apaf1 and dATP form an apoptosome
4. The apoptosome activates caspase 3
5. Caspase 3 does the rest
What are the two ways that the intrinsic and extrinsic pathways of apoptosis can converge?
1. They can converge at the level of caspase 3.

2. They can converge because caspase 8 can cause make tBid from Bid. This interacts with BAX to start the intrinsic pathways to start.
What accumulates in autophagic cell death?
Autophagic vacuoles
What causes the accumulation of autophagic vacuoles?
Specific inhibition or activation of autophagy
What does specific inhibition of autophagy cause?
Prevents the recycling of components back to the mitochondria for normal function
With autophagy, what happens to the number of mitochondria present?
Does autophagy have a potential role in neurodegenerative disease?
What does AB come from?
Amyloid precurson protein (APP)
What forms plaques in AD?
What eventually leads to cell death in AD?
The accumulation of AB plaques (from APP).
What are the three challenges of studying cell death in AD?
1. Correlating in vitro/animal models with human AD
2. Chronic onset and progression
3. The amount of cell death at any one time is minimal