C. Brain Damage and Neuroplasticity Part 3 Flashcards

1
Q

In patients w/Alzheimers disease their brains tend to have a build-up of ___________ within the neurons and ____________ outside the neurons.

A

neurofibrillary tangles, amyloid plaques

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2
Q

Describe the following terms wrt Alzheimer’s. Which ones are found inside vs outside the cell?
a) neurofibrillary tangles
b) amyloid plaques

A

a) a clumping of the phosphorylated tau protein (inside)
b) when an amyloid precursor protein (APP) is cleaved incorrectly resulting in an accumulation of Abeta (outside)

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3
Q

In a healthy individual, what is the fxn of the following?
a) tau protein
b) APP (amyloid precursor proteins)

A

a) holds together the microtubules of the neuron
b) results in membrane maintenance

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4
Q

Why do ppl diagnosed w/ down syndrome have a higher likelihood of developing early-onset Alzheimer’s?

A

the amyloid plaques that are produced by the APP are associated w/ chromo 21. Thus since ppl diagnosed w/ down syndrome have 3 chromo 21s they are likely to produce more plaques than those who have 2 chromo 21s

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5
Q

T or F - tangles and plaques are evenly spread across the whole brain

A

F - they are widely spread however they tend to accumulate in certain brain regions

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6
Q

Name 3 brain regions that are affected by the neurodegeneration of Alzheimer’s

A
  1. enlarged ventricles (make the hole bigger)
  2. shrinkage of the cerebral cortex (edge of the brain)
  3. shrinkage of hippocampus
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7
Q

Name the 2 forms of Alzheimer’s Disease and ANS the following; Which is least common?
a) how many mutations are associated?
b) do they involve genes for the amyloid and/or tau?
c) Provide an example

A
  1. early onset = familial/inherited (least)
    a) 4
    b) amyloid
    c) APP or PSEN
  2. late-onset = general mutation due to exp
    a) +15
    b) amyloid + tau
    c) APOE
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8
Q

Describe ppl that are referred to a ‘high plaque normal’.

A

ppl w/ an INC number of plaques in their brain but exp no Alzheimer’s symptoms

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9
Q

What are the 2 treatments used to alleviate the symptoms of Alzheimer’s?

A
  1. cholinesterase inhibitors = ACh agonist used to INC ACh lvls
  2. immunotherapy = vaccines used to work against amyloid proteins
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10
Q

Why would INC levels of ACh alleviate the symptoms of Alzheimer’s?

A

ACh is associated w/ learning and mem which ppl w/ Alzheimer’s lack thus INC the lvls who hopefully maintain some of those cog processes

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11
Q

Describe Transgenic animal models. What are the advantages and disadvantages of using these models to help treat Alzheimer’s

A

a) they are animals that have the genes of another species
b) A = can transplant the genes that are associated w/ Alzheimer’s to mimic the symptoms and hopefully learn more about the disease
c) D = Researchers are only well versed in the familial form of this disease (early onset) which only 1% of ppl w/Alzheimer’s get. Thus the results may not be accurate for the late-onset form

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12
Q

In the object recognition task study that involved comparing transgenic mice that mimic Alzheimer’s, there were two groups. What were they?

A

a) 5XFAD = Abeta plaque gr
b) 3xTG = Abeta plaque + tangle gr

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13
Q

When the AD (Alzheimer’s disease) trangenic mouse models in each group were studied for cog deficits, they measured the males and females separately. Why?

A

B/c there is a difference in sex wrt to this disorder.

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14
Q

In the object recognition test used by AD transgenic mouse models both long-term and short-term mem was measured for both males and females. What were the results for each gr (5xFAD, 3xTG) wrt the following;
a) short-term mem males
b) long-term mem males
c) short-term mem females
d) long-term mem females

A

5xFAD - just plauques
a) good mem
b) impaired mem
c) impaired mem
d) impaired mem

3xTG - plaques + tangles
a) good mem
b) impaired mem
c) good mem
d) impaired mem

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15
Q

Describe the 4 neuroplastic responses to the NS?

A
  1. neural degeneration = deterioration and death of a neuron
  2. regeneration = the regrowth of a damaged neuron
  3. reorganization = the reorganization of neural connections due to damage or exp
  4. recovery = fixing a damaged neuron
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16
Q

When do the two types of neural degenerations occur?

A
  1. neurodegenerative diseases = dying
  2. neurodevelopment = pruning
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17
Q

T or F - neural degeneration is always bad as it involves killing off neurons and their connecitons

A

F - during neurodevelopment neural degeneration occurs in order to make the networking in the brain more efficient

18
Q

Describe axotomy models. What happens in the 3 following cases? When do these cases happen, always, sometimes, or often?
a) anterograde degeneration
b) retrograde degeneration
c) transneuronal degernation

A

Axotomy model = cutting the axon of a neuron as seeing what happens
a) the rapid deterioration of the distal segment (axon terminal part) (always)
b) the slow deterioration of the proximal segment (dendric and soma part) (often)
c) damage to a neuron that was connected to an already degraded neuron due to lack of connectivity (sometimes)

19
Q

It’s stated that transneuronal degeneration can be either anterograde or retrograde. What does this mean?

A

the neuron degenerating can be the neuron before or after the already degenerated neuron (neuron that was cut)

20
Q

Match the following terms to the image
a) retrograde degeneration
b) axotomy
c) anterograde degenertation
d) transneuronal

A
21
Q

T or F - neural regeneration is common and very precise in invertebrates and lower vertebrates

A

T

22
Q

Which type of NS does neural regeneration show itself wrt higher vertebrates

A

PNS due to is being a very imprecise process

23
Q

How do the following support cells w/in the CNS/PNS prevent/promote neuronal regeneration
a) oligodendroglia - 4
b) Schwann - 4

A

a)
- don’t clean cellular debris
- don’t guide regeneration at all
- astrocytes form glial scars
- astrocytes release factors that inhibit regeneration
b)
- clean cellular debris
- produce neurotrophic factors that stim growth
- use physical traps to guide successful connections
- proliferate (multiply) to produce more Schwann cells

24
Q

The following images demonstrate the 3 patterns of axonal regeneration in mammals w/in the PNS.
a) Describe what is happing in each case
b) How does this explain why regeneration doesn’t happen within the CNS?

A

a) in the image
b) Dep on the severity of the damage for instance the 3rd case, there may be regeneration in which the axons reattach however it is a very imprecise process that could result in incorrect connections. This would be very bad for the CNS

25
Q

T of F - Unlike the PNS there is no way for the CNS to even remotely regenerate lost connections b/w neurons due to the inability to regenerate damaged neurons

A

F - non damaged neurons can collaterally sprout to healthy neurons that were connected to the damaged neuron to form new connections

26
Q

a) What is this image demonstrating
b) Where is this occurring?

A

a) collateral sprouting
b) CNS

27
Q

What are the 2 factors that promote the reorganization of neurons?

A
  1. strengthening existing connections due to experience
  2. establishing new connections due to damage
28
Q

When someone states that neurons are ‘greedy’ what does this mean?

A

This means that neurons will take over areas that are damaged or disconnected neuronal networks as their own.

29
Q

Wrt reorganization what would happen if a person damaged their visual cortex to the point of becoming blind?

A

there would be an INC in the auditory and somatosensory cortices as they would take over that visual cortex. This would result in enhanced auditory and somatosensory skills

30
Q

Describe cross-modal neuroplasticity. which of the following neuroplastic responses does this idea relate to?
a) neural degeneration
b) regeneration
c) reorganization
d) recovery

A

c) - The act of one damaged modality (sense) being taken over by another

31
Q

What are the ways thought to be involved w/ strengthening existing connections wrt the reorganization of neurons?

A
  1. releasing the inhibition of certain non-damaged neuronal connections due to the original connecting being damaged
  2. collateral sprouting = alive neurons taking over damaged neuronal connections
32
Q

T or F - wrt neuronal damage improvements and recovery of neurons are interchangeable terms

A

F - improvement discusses the act of fighting the symptoms of damage vs recovery where you health those damaged parts

33
Q

What are 3 cases that can cause true recovery of neurons in the CNS?

A
  1. collateral growth
  2. neuroplastic changes in undamaged tissue
  3. neurogenesis from stem cells
34
Q

What are 2 ways to improve neural damage in the CNS?

A
  1. alleviate symptoms
  2. cognitive reserve (idea that keeping your brain busy will strengthen its ability to fxn as a whole)
35
Q

Describe what happened in the Nun study wrt the cognitive reserve theory

A

Nuns all had severe pathology of those w/Alzheimer’s in their brain however they showed no symptoms. This is probably due to them keeping their minds busy learning new things over their lifespan

36
Q

In the Ninja warrior mice cognitive reserve experiment they took young mice with Alzheimer’s pathology and put them in different conditions. standard housing, enrichment housing, control track, and enrichment track. After some time they had the mice undergo the spontaneous object recognition test to test their memory. What were the results of this test for each group? What did this show overall? Why may these not be the most reliable results?

A

a)
- SH + CT = impaired object mem
- ET + EH = intact mem
b) the enriched environments caused compensatory changes w/in the mind which lessened the severity of alzhiemer’s
c) all the mice were males but Alzheimer’s is shown to be more prevalent in females

37
Q

What are the 2 ways to promote recovery following CNS damage?

A
  1. exercise + enrichment of exp
  2. rehabilitative training
38
Q

Describe the 3 types of CNS damages that can be treated using rehabilitative training.

A
  1. strokes = physical repetitive training of specific activities in order to save the penumbra
  2. spinal injuries = gradually re-learning how to walk by walking on a treadmill and INC the pressure over time
  3. phantom limb = mirror box - look at reflection in order to see both limbs and move real limb out of the painful position
39
Q

What was Ramachandran’s hypothesis? What type of treatment did he come up w/?

A
  1. phantom limb is caused by the reorganization of the somatosensory cortex following an amputation not the nerve endings at the site of the amputation
  2. mirror box = using the reflection to make the brain believe that you have 2 limbs again and them moving the real limb out of the painful position
40
Q

Strokes are caused by
a. tardive dyskinesia.
b. cerebral hemorrhage.
c. cerebral ischemia.
d. all of the above
e. both B and C

A

e

41
Q

In the event of a stroke, describe the two regions where tissue damage occurs. What is the role of the neurotransmitter glutamate in brain damage caused by stroke? Theoretically, how might one limit the extent of this damage?

A

a) Infarct: region of dead or dying tissue
b) Penumbra: region of dysfunctional tissue surrounding infarct may eventually die off without intervention
c) Glutamate toxicity: Dying neuron releases
an excess of glutamate; glutamate triggers
excessive Na+ and Ca++ ion influx into post-synaptic
neurons; excessive ion influx kills post-synaptic
neuron, which before dying also releases glutamate
and cause further brain damage
d) Limit damage in penumbra with glutamate receptor antagonists/“blockers”, specifically NMDA receptor antagonists