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neuro 210 finallll > Cell Death in CNS > Flashcards

Cell Death in CNS Flashcards

1
Q

What are the many different causes of cell death (7)?

A
  • development (normal)
  • trauma
  • toxins (e.g. alcohol, pesticides, heavy metals)
  • cerebral vascular disease
  • infectious agents
  • genetic diseases
  • neurodegenerative diseases of unknown cause
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2
Q

What is multi-infarct dementia?

A

occurs when people have small mini strokes over time

  • can cause or lead to dementia
  • its temporary/transient strokes but has major overall consequences
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3
Q

what is Pick’s disease

A

its a cause of frontotemporal degeneration

  • affects frontal and anterior temporal lobe areas
  • posterior parts of the brain are undamaged
  • causes atrophy and gyro become thinner and sulci deepen … cerebral ventricles become huge because surrounding tissue died off
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4
Q

What is huntington’s disease and how does it look like?

A

genetic disease

  • shrinking of caudate nucleus and basal ganglia because of cell death
  • ventricles are not round around the edges because its been dying off
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5
Q

how does parking sons disease look like in the brain?

A

less neural tracts in the substantia nigra compared to normal people

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6
Q

What is advanced CJD? how does it look like in the brain?

A

its mad-cow disease and brain cells die and look like sponge (bc of holes) and the brain overall has shrunked

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7
Q

what is meningioma?

A

tumor in the meningial linings
- its banging by itself but it cause harm to the brain if it keeps growing because its heavy and has a lot of pressure on the brain. it causes something called mass effect which is dents in the brain

it also compresses blood vessels and decreases blood flow to area

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8
Q

What is a brain that has alzheimers look like?

A

its shrunken

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9
Q

what does a brain of a person with alcoholism look like?

A

its very shrunken even more than alzheimers

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10
Q

how does the fetal alcohol brain look like?

A

its shrunken and slow development

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11
Q

What happens at a cellular level in neurons and glia?

A
  • neurons are much more vulnerable than glia
  • brain consumes 25% total oxygen and glucose in the blood stream
  • neurons use glucose as their primary carbon source
  • neurons are not replaced in significant numbers (but glia are)
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12
Q

What are some forms of appropriate cell death?

A

developmental die off –> appropriate

  • during development, more neurons than will be needed are born
  • fine tuning of connections orchestrated by interactions with the environment
  • developmental cell death occurs without tissue inflame or disruption of surrounding cells
  • use it or lose it principle that involves growth factors and electrophysiological activity
  • this type of cell death is programmed by the DNA for establishment of the CNS and its appropriate
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13
Q

What is inappropriate cell death?

A

injury to the brain is any stimulus that brings changes in cell physiology and/or anatomy - internal or external

  • injury can be reversible or irreversible
  • adaptation results from the changes in cell due to reversible injury ONLY
  • irreversible injury results in cell death
  • whenever something takes neurons out of homeostasis state, it can result in cell death if the cell can fully adapt to the stimulus its reversible injury but if not, it will become irreversible and cause cell death (like stroke or head trauma)
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14
Q

What is glutamate-induced neuronal death?

A

also called excitotoxicity
- an event has caused cellular energy failure: disturbance causing lack of oxygen or glucose to cell (i.e. trauma or stroke)

this is excessive stimulation through receptors for neurotransmitter glutamate

  • caused by excessive release, and failure of glutamate uptake mechanisms
  • too much glutamate activity causes an imbalance of other ions such as calcium and sodium which results in cell death
  • this will cause both DNA programmed and necrotic cell death
  • glial cells clean up glutamate but they need ATP without o2 theres no ATP for glia theres no ATP for glia
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15
Q

What is reactive oxygen species cell death?

A

cell death caused by free radicals of oxygen

  • will damage cell membranes and intracellular organelles
  • will activate DNA programmed cell death mechanisms
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16
Q

What is hypoglycaemia causing cell death?

A

low glucose levels

  • loss of glucose leads to rapid depletion of cellular energy reserves
  • will activate DNA programmed cell death mechanisms
17
Q

What are some ways that free radicals are formed? (6)

A
  1. ionizing radiation
  2. smoking
  3. air pollution
  4. inflammation
  5. metabolism
  6. UV light
18
Q

What are two main modes of inappropriate cell death?

A
  1. necrosis –> rapid, somewhat messy death via induced inflammation
  2. apoptosis –> programmed cellular suicide … has a window of opportunity of recovery unlike necrosis and its slower
19
Q

What is Necrosis?

A

dramatic and very rapid form of cell death in which every compartment of the cell disintegrates… outer cell membrane ruptures and releases its intracellular contents

20
Q

what is necrosis characterized by?

A

dysregulation of ion homeostasis (dissociation between inner and outer membrane) causing:

  1. cell swelling
  2. dilation of mitochondria and ER
  3. formation of vacuoles in cytoplasm
  4. activation of enzymes called proteases, which degrade cellular components (normally these proteases are held in lysosome packages but necrotic process release them) proteases cause neighbouring cells to rupture and inflammatory agents to start moving into those regions
21
Q

What happens during cell death in necrosis?

A
  • chromatin clumps and nuclear membranes are disrupted
  • gene transcription and protein synthesis stops
  • ATP is rapidly depleted
  • cells lyse and spill their contents into the ECF
  • contents can damage neighbouring cells
  • spillage causes inflam response
22
Q

What kind of cells go through necrosis and apoptosis.. what does it depend on?

A

there are very few cell deaths that trigger only capable of inducing either necrosis or apoptosis, they usually occur together

whether a cell undergoes apoptosis or necrosis is determined primarily by the intensity and/or duration of the death-inducing stimulus

  • if a stimulus is severe and/or sustained it will induce necrosis (i.e. glutamate/excitotoxicity)
  • if stimulus is less severe with transient stresses (comes and goes) it will induce apoptosis (i.e. energy failure/ischemia)
23
Q

What is the process of Apoptosis (aka Type 1 PCD)?

A

there are multiple forms of programmed cell death (PCD) but apoptosis is the best characterized form of it

  • apoptosis occurs in both appropriate and inappropriate cell death (i.e. like during development)
24
Q

What are two main pathways of apoptosis?

A
  1. intrinsic –> generated by signals arising within the cell
  2. Extrinsic –> triggered by death activators binding to receptors at the cell surface

both pathways join together to make a final common pathway

there is also a direct-to-DNA pathway called Caspase-Independent pathway (doesn’t require intrinsic or extrinsic enzymes)

25
Q

In the intrinsic (mitochondrial) pathway what is the bcl-2 family of cells and what do they activate?

A

the bcl-2 family promotes apoptosis (pro-apoptotic) and they activate caspases (cytosine-dependent, aspartate-specific proteases) which are program executors of apoptosis

26
Q

What happens in the mitochondria in the intrinsic pathway?

A

the pro-apoptotic winner causes a pore to open in the mitochondria via changed permeability

  • out of the pore leaks CYTOCHROME C
  • cytochrome c binds with molecule called apoptosis activating factor-1 (APAF-1) and induces it to creat the first stage of an apoptosome
  • together APAF-1 and Cytochrome C capture and bind caspase-9 which completes the apoptosome
  • if nothing stops the program at this stage, the apoptosome will progress to the next step… which is activation of the final step caspase-3
27
Q

What are the summarized steps of intrinsic pathway?

A

apoptotic stimuli –> bcl-2 family war in the mitochondria –> cytochrome release –> cytochrome c binds with APAF-1 factor –> APAF 1 and CC activate caspase-9 –> caspase 9 activates caspase 3 –> cell death

28
Q

What is the extrinsic pathway?

A

also known as death receptor pathway because it includes death receptors (Fas, TNF, Drs) which are proteins embedded through the cell membrane with their receptor domains exposed at the cell surface

29
Q

what is the Fas receptor?

A

its the best characterized death receptor… Fas ligand (FasL) binds at this receptor, this binding causes activation o the receptor and its death domains

30
Q

What happens after Fas receptor is activated?

A

it recruits caspase-8 in pro-from and then the binding of death domain and caspase 8 cause activation of caspase 8

the activated caspase-8 then proceeds with the death plan by activating the final death effector caspase-3 (same as the intrinsic)

31
Q

How do the extrinsic and intrinsic pathway interact?

A
  • the extrinsic pathway does have a mechanism to interact with the intrinsic pathway that involves caspase-8 because caspase-8 can activate a pro-apoptotic molecule typically associated with the intrinsic apoptotic pathway thus the two pathways can work towards death simultaneously
32
Q

what is the summary of the extrinsic pathway?

A

pro-apoptotic ligand binds to fas death receptor –> causes release of caspase 8 and activation of it –> causes activation of caspase 3 –> apoptosis

33
Q

How does the caspase-independent pathway get activated?

A

through the apoptosis inducing factor AIF…

AIF normally located in the inter membrane space of the mitochondria
- when cell receives signal to die (i.e. ROS) AIF is released from mitochondria, and it migrates to the cell nucleus and binds to DNA and triggers destruction of DNA and cell death

this is independent of the enzymes used in intrinsic and extrinsic pathways

the AIF gets released when permeability changes from the pores of the mitochondria

34
Q

What is the difference between apoptosis vs. Necrosis?

A

two processes are temporally dislocated and likely represent two extremes of a continuum
- necrosis process cans tart only and exclusively when the cell DIES and is an irreversible process with no return

death of cells is immediate in necrosis but it takes time in apoptosis

one of the main differences is that in apoptosis, the membrane is still intact and structurally ok but in necrosis it just explodes

35
Q

What are some common diseases associated with apoptosis in the form of cancers, autoimmune disorders and viral infections?

A
  1. cancers –> follicular lymphomas, carcinomas, hormone dependent tumors, breast/ovarian/prostate cancer
  2. autoimmune disorders –> systemic lupus –> immune mediate glomerulonephritis
  3. Viral infections –> herpes, poxvirus, adenoviruses
36
Q

What are diseases associated with increase apoptosis in terms of neurodegenerative disorders, ischemic injuries and viral infections?

A
  1. neurodegenerative disorders –> alzhimers, parkngsons, amyotrophic lateral Sclerosis (ALS) and retinitis pigments
  2. ischemic injury like stroke, myocardial infarction, reprefusion injury
  3. viral infection: AIDS and toxin induced liver diseases from alcohol
37
Q

What is black death?

A

its frost bite from loss of glucose due to loss of blood to an area of the body.. black death of necrosis ruptures and spills ICF contents turning body parts black

38
Q

What are most common assays (determining biochemical and immunological activity) for apoptosis?

A
  1. cytomorphological changes
  2. dna fragmentation
  3. detection of caspases, cleaved substrates, regulators and inhibitors
  4. membrane alterations
  5. mitochondrial assays (biochemical and immunological activity)
39
Q

What is tunnel staining?

A

terminal deoxynucleotidyl transferase mediated dUTP nick end labeling.. looks for breaks in DNA and visualizing it to check for apoptosis

neuro 210 finallll (12 decks)

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