C. Brain Damage and Neuroplasticity Part 3 Flashcards
In patients w/Alzheimers disease their brains tend to have a build-up of ___________ within the neurons and ____________ outside the neurons.
neurofibrillary tangles, amyloid plaques
Describe the following terms wrt Alzheimer’s. Which ones are found inside vs outside the cell?
a) neurofibrillary tangles
b) amyloid plaques
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)
In a healthy individual, what is the fxn of the following?
a) tau protein
b) APP (amyloid precursor proteins)
a) holds together the microtubules of the neuron
b) results in membrane maintenance
Why do ppl diagnosed w/ down syndrome have a higher likelihood of developing early-onset Alzheimer’s?
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
T or F - tangles and plaques are evenly spread across the whole brain
F - they are widely spread however they tend to accumulate in certain brain regions
Name 3 brain regions that are affected by the neurodegeneration of Alzheimer’s
- enlarged ventricles (make the hole bigger)
- shrinkage of the cerebral cortex (edge of the brain)
- shrinkage of hippocampus
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
- early onset = familial/inherited (least)
a) 4
b) amyloid
c) APP or PSEN - late-onset = general mutation due to exp
a) +15
b) amyloid + tau
c) APOE
Describe ppl that are referred to a ‘high plaque normal’.
ppl w/ an INC number of plaques in their brain but exp no Alzheimer’s symptoms
What are the 2 treatments used to alleviate the symptoms of Alzheimer’s?
- cholinesterase inhibitors = ACh agonist used to INC ACh lvls
- immunotherapy = vaccines used to work against amyloid proteins
Why would INC levels of ACh alleviate the symptoms of Alzheimer’s?
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
Describe Transgenic animal models. What are the advantages and disadvantages of using these models to help treat Alzheimer’s
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
In the object recognition task study that involved comparing transgenic mice that mimic Alzheimer’s, there were two groups. What were they?
a) 5XFAD = Abeta plaque gr
b) 3xTG = Abeta plaque + tangle gr
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?
B/c there is a difference in sex wrt to this disorder.
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
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
Describe the 4 neuroplastic responses to the NS?
- neural degeneration = deterioration and death of a neuron
- regeneration = the regrowth of a damaged neuron
- reorganization = the reorganization of neural connections due to damage or exp
- recovery = fixing a damaged neuron
When do the two types of neural degenerations occur?
- neurodegenerative diseases = dying
- neurodevelopment = pruning
T or F - neural degeneration is always bad as it involves killing off neurons and their connecitons
F - during neurodevelopment neural degeneration occurs in order to make the networking in the brain more efficient
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
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)
It’s stated that transneuronal degeneration can be either anterograde or retrograde. What does this mean?
the neuron degenerating can be the neuron before or after the already degenerated neuron (neuron that was cut)
Match the following terms to the image
a) retrograde degeneration
b) axotomy
c) anterograde degenertation
d) transneuronal
T or F - neural regeneration is common and very precise in invertebrates and lower vertebrates
T
Which type of NS does neural regeneration show itself wrt higher vertebrates
PNS due to is being a very imprecise process
How do the following support cells w/in the CNS/PNS prevent/promote neuronal regeneration
a) oligodendroglia - 4
b) Schwann - 4
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
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) 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