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NEUR 350 > Repair & Regeneration > Flashcards

Repair & Regeneration Flashcards

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1
Q

What is the functional recovery of the brain?

A

reorganization of intact circuits

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2
Q

In stroke patients, the movements of the impaired hand showed what on the fMRI scan?

A

significant activations in the ipsilateral (opposite side of the lesion) motor areas
*plasticity and reorganization for functional recovery

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3
Q

What do fMRI scans of diminished activity in stroke patients show?

A

amount of cortical diminished activity declines with improved function (movement)

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4
Q

What is CTE?

A

chronic traumatic encephalopathy
brain injury resulting from repetitive traumatic forces to the head

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5
Q

What is stage 1 of CTE?

A

no symptoms
isolated spots of tau build mostly around the frontal lobe

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6
Q

What is tau?

A

a protein in the brain that builds up in CTE
forms around blood vessels, interrupting normal functioning and eventually killing nerves

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7
Q

What is stage 2 of CTE?

A

rage, impulsivity, depression
symptoms being to appear as defective tay protein affects more nerve cells in the frontal lobes

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8
Q

What is stage 3 of CTE?

A

confusion, memory loss
tau deposits expand from the frontal lobes to temporal lobes
the condition begins to affect the amygdala (emotion) and hippocampus (memory)

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9
Q

What is stage 4 of CTE?

A

advanced dementia
tau deposits have overwhelmed the brain, killing many nerve cells and shrinking the brain by roughly half its mass
the brain becomes deformed and brittle, and cognitive function is severely limited

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10
Q

How has CTE diagnosis changed?

A

could only diagnose after death
now PET imaging can show tau deposition in aging brains

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11
Q

How does PET imaging show tau deposits?

A

uses a beta-amyloid precursor
in older adults, increased beta-amyloid is associated with increased tau deposits
the large increase in tau deposits with Alzheimer’s

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12
Q

What are the eight stages in axotomy?

A
  1. terminal degeneration
  2. Wallerian degeneration
  3. myelin debris
  4. microglia (CNS) or macrophage (PNS) infiltration
  5. chromatolysis
  6. retraction of synaptic terminals and glial cells
  7. transneuronal degeration (retrograde)
  8. transneuronal degeration (anterograde)
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13
Q

What is Wallerian degeneration?

A

an active process of degeneration that is irreversible

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14
Q

What is chromatolysis?

A

the cell body swells, and the nucleus moves to an eccentric position
ER fragmented

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15
Q

What is the difference between phagocytic infiltration in PNS vs CNS?

A

PNS - rapid process, macrophages dispose of debris
CNS - oligodendrocytes cant dispose of debris (depends on resident microglia cells)

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16
Q

How does axotomy affect other neurons?

A

synaptic inputs and targets can atrophy and degerate
*impair functional recovery (synaptic stripping)

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17
Q

What is the core pathway that regulates axotomy in mice?

A

NMNAT2 is present in the axon
it generates NAD
which promotes high ATP, low Ca2+
= axon integrity

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18
Q

How is the core pathway that regulates axotomy affected by injury in mice?

A

NMAST2 breaks down rapidly (unstable)
causes a decrease in NAD generation
causing low ATP, high Ca2+
= axonal degeneration

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19
Q

What is the role of SARM in the core pathway that regulates axotomy in mice?

A

uninjured mice - NMNAT2 acts to inhibit SARM1
injured mice - break down of NMNAT2 uninhibited SARM1, allowing it to break down NAD (further contributing to axonal degeneration)

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20
Q

Why doe axons in the PNS regenerate better than those in CNS?

A

PNS
- perineural sheath reforms rapidly, and Schwann cells in the distal stump promote axonal growth by producing trophic and attractant factors and expressing high levels of adhesion proteins
CNS
- distal segment disintegrates, and myelin fragments
- reactive astrocytes and macrophages are attracted to the lesion site, creating a glial scare that inhibits axonal regeneration

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21
Q

What is the glial scar?

A

dramatic overgrowth
local decrease in inflammatory mediators
imposes neuronal growth

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22
Q

What is the cellular response to injury in the CNS?

A
  • degeneration of myelin and other cellular components
  • clearing of debris by microglia - act as phagocytic cells
  • local production of inhibitory factors by astrocytes, oligodendroglia and microglia
  • glial scar formation
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23
Q

What is the timeline of mediator cells in response to CNS injury?

A

DAMPs, cytokines, chemokines -> neutrophils -> monocytes -> microglia, astrocytes -> T and B cells

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24
Q

What does local damage cause cytokines and other molecules to activate?

Study These Flashcards
A

microglia and astrocytes
- astrocytes increase in frequency to form a local glial scar

25
What cells rapidly infiltrate when the BBB is compromised?
neutrophils and other monocytes - release additional pro-inflammatory cytokines that elicit a more robust astrocyte response and reinforce local inflammation
26
What does the local reinforcement of inflammation when the BBB is compromised lead to?
an additional decrease in the potential for preserving neuronal survival, tissue integrity, and the possibility for modest regrowth and repair
27
What is one of the roles proved in microglial response to local brain injury?
block and contain damage (decrease lesion size)
28
What is the result of inserting a peripheral nerve graft to bypass the CNS lesion?
promotes regeneration of both ascending and descending axons - provides a favourable environment for the regeneration of central axons
29
How do PNS and CNS nerves differ in their ability to support axonal regeneration?
PNS - severed axons regrow past the site of injury CNS - severed nerve axons fail to regrow past the site of injury
30
What occurs if you insert a segment of CNS nerve into the PNS?
insertions of the CNS nerve suppress the ability of the PNS nerve to regenerate
31
What occurs if you insert a segment of the PNS nerve into the CNS?
promotes regeneration
32
How does myelin inhibit the regeneration of central axons?
when peripheral branches were sectioned, the central branches of the sectioned axon degenerated - little regeneration occurred with myelin-rich cord - when myelin was blocked, sensory fibres that entered neighbouring uninjured nerve roots sprouted new collaterals
33
What are the two ways glial scar hinders axonal regeneration?
- mechanical interference (proliferation of glial cells) - inhibitory proteins produced (myelin)
34
What three proteins are exposed when myelin breaks down during injury and what is their role?
Nogo-A OMgp MAG - bind to membrane receptors (PirB, NogoR) that act on p75 receptor to inhibit axonal regeneration
35
What is CSPG's role in the glial scar?
major components of the glial scar and are thought to surpass axon regeneration through interaction with the PTP-sigma receptor (actiat
36
What are the two obstacles to nerve growth in the extracellular space?
1. chondroitin sulphate proteoglycan (CSPG) molecules, which have a backbone and many side branches that block the way 2. special cell-membrane- anchored proteins that actively stop growing nerve fibres (Nogo)
37
What is the bacterial enzyme chondroitinase ABC's role in clearing the way for growing nerve fibres?
can prune side chaines of CSPG's
38
How can Nogo be blocked to clear the way for growing nerve fibres?
by specific antibodies
39
How can a conditioning lesion promote regeneration of the central branch?
if a peripheral branch is sectioned before the central branch is damaged, the latter will grow beyond the lesion site
40
How can the impact of a conditioning lesion be mimicked?
elevating levels of cAMP or GAP-34 in the peripheral branch
41
How does nerve growth potential change with age?
decreases
42
What is the result when the SOCS3 gene is deleted?
allows CNTF to activate CP130 which acts on JAK/STAT to promote regeneration *typically SOCS3 inhibits GP130
43
What is the result when the PTEN gene is deleted?
Allows mTOR to promote regeneration *PTEN typically inhibits mTOR
44
How can functional recovery be achieved after spinal cord injury?
severed corticospinal axons can re-establish connections with motor neurons by sprouting axon collaterals that innervate propriospinal interneurons whose axons bypass the lesion and contact motor neurons past the lesion site
45
How is the motor cortex-brainstem relay recovered after spinal cord injury?
neuromodulation and rehab training coax the cortex into re-establishing connectivity with the spinal cord by enhancing the formation of circuits between the cortex and vGi (brainstem), and the vGi and the spinal cord below the level of injury
46
When should rehab be introduced after injury?
immediately
47
What are the five developmental stages of adult neurogenesis in the dentate gyrus (hippocampus)?
1. proliferation ~25 hr 2. differentiation ~4 days 3. migration 4. axon/dendrite targeting ~4-10 days 5. synaptic integration ~2-4 weeks
48
Explain stage 1: the proliferation of adult neurogenesis
- stem cells with their cell bodies are located in the subgranular zone and have radial processes that project through the granular cell layer and shot tangential processes that extend along the granule cell layer and hilus - multipotent neural stem cells give rise to intermediate precursor 'transient amplifying cell' that divide asymmetrically - after each cell division, a transient amplifying cell that reenters the cell cycle for an additional round of asymmetric division
49
Explain stage 2: the differentiation of adult neurogenesis
- postmitotic neuroblasts differentiate into mature neurons - proliferating progenitors in the SGZ are tightly associated with astrocytes and vascular structures
50
Explain stage 3: the migration of adult neurogenesis
immature neurons migrate a short distance into the granule cell layer
51
Explain stage 4: the axon/dendrite targeting of adult neurogenesis
- immature neurons extend their axonal projections along mossy fibre pathways to the CA3 pyramidal cell layer - they send their dendrites in the opposite direction toward the molecular layer
52
Explain stage 5: the synaptic integration of adult neurogenesis
new granule neurons receive inputs from the entorhinal cortex and send output to the CA3 and hilus regions
53
What does the loss of dopaminergic neurons in the substantia nigra in Parkinson's cause?
deprives the putamen-globus pallidus pathways of their drive
54
What is the role of dopaminergic projections from the substantia nigra?
innervate the putamen, which in turn activates neurons in the globus pallidus - pallidum output facilitates movement
55
How can loss of dopaminergic neurons in Parkinsons be treated?
- direct injection of embryonic dopaminergic neurons into the putamen reactivates the globus pallidus output pathways
56
What are pluripotent stem cells?
- generated from patients' skin cells (no risk of rejection) - can be guided to any cell type through the introduction of certain precursors in culture and then implanted to complete differentiation and integrate into function circuits
57
How can pluripotent stem cells differentiate into spinal motor neurons in an ALS patient?
iPS cells were directed to a motor neuron fate - skin fibroblasts -> reprogrammed to iPS cells -> retinoic acid -> motor neurons
58
How can demyelinate axons restore myelination?
transplantes oligodentrocyre stem cells grafts if oligodendrocyte precursor cells can restore myelination to near-normal

NEUR 350 (11 decks)

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