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NEURO 411 > Pathological Spreading of Disease > Flashcards

Pathological Spreading of Disease Flashcards

1
Q

Propagation is the _______________ of protein aggregates from one cell to another followed by _____________ of aggregation int eh receiving cell.

A

transmission; seeding

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2
Q

What are the requirements for transmission?

A
  • RELEASE from cell
  • compartment/entry point BIG ENOUGH to allow for transport of the seed
  • uptake by a CONNECTED CELL (major factor is distance)
  • delivery into a SUITABLE COMPARTMENT in recipient cells
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3
Q

What are the requirements for seeding?

A
  • seed in CORRECT compartment
  • AVAILABLE MONOMER for formation of new aggregates
  • STABLE SEED that can maintain shape and not be degraded
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4
Q

What are the factors affecting spreading of variant aggregates?

A
  • ability to seed
  • ability to be transmitted
  • ability to avoid degradation
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5
Q

What aspect of the aggregate may be key to which pathology develops?

A

shape

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6
Q

TRUE or FALSE: the same protein will lead to the same NDD, even if the shape is different

A

FALSE: different shapes can lead to distinct NDD

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7
Q

What was the difference in seeding observed in the experiment where tau aggregates were injected into mice hippocampus? Which seeds produced glial pathology?

A
  • AD and CBD = low seeding
  • PSP = high seeding (more positive staining)
  • CBD and PSP seeds –> glial pathology
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8
Q

TRUE or FALSE: in the experiment where tau aggregates were injected into mice hippocampus, each seed produced pathology in DISTINCT brain regions and patterns, despite injection into the SAME brain area

A

TRUE

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9
Q

What are the prion diseases in humans, sheep, and cows?

A
  • humans = KURU by ingesting infected human brain
  • sheep = SCRAPIE by ingesting infected feed or env contamination
  • cow = MAD COW DISEASE by ingesting contaminated feed
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10
Q

How is it possible that ingesting prions can lead to a NDD?

A
  1. prions can survive acidic environment of the gut
  2. cross epithelial layer
  3. interact with immune cells
  4. bind FDC
  5. transmit to nerve fibers (due to proximity)
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11
Q

What harsh conditions does PrPsc need to survive the gut environment and passage through cells?

A
  • acidic pH of gut, which normally denatures most proteins
  • proteases function to break down proteins we ingest
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12
Q

Why might FDCs be efficient at PrPsc propagation?

A

they express sufficient levels of PrPc

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13
Q

What are the first neurons that allow PrPSc into the nervous system?

A

neurons of the ENTERIC nervous system

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14
Q

TRUE or FALSE: PrPc is more stable than PrPSc

A

FALSE: PrPSc fibrils are more stable than its expressed monomer form, PrPc

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15
Q

___________ might trigger alpha-synuclein pathology

A

inflammation

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16
Q

PD patients report ____________ issues decades before motor symptoms related to neurodegeneration?

A

gut/intestinal

17
Q

synuclein aggregates may be formed in ________________ then get tranmitted to ___________.

A

enteric neurons; vagus nerve

18
Q

TRUE or FALSE: vagotomy increases risk of developing PD

A

FALSE: decrease

19
Q

TRUE or FALSE: there is evidence that people have gotten PD from ingesting infected tissue

A

FALSE: only seen in prions diseas

20
Q

What were the main findings of the study that investigated injection of alpha-synuclein aggregates into the mouse gut?

A
  • mice that did not get synuclein and mice that had a vagotomy did not have any synuclein pathology in the brain
  • only WT mice had neurodegeneration
  • it is possible for aggregation to start in the gut and travel to the brain
21
Q

Why is the origin point usually the same for a disease?

A

VULNERABILITY of certain neuronal/cell populations to protein misfolding and release of aggregates

22
Q

What are some example of factors that could influence aggregate formation, causing the same origin point for the same disease?

A
  • proteins that are expressed, which allow for initial aggregation
  • protein degradation capacity of cell
  • activity and environment of cell
23
Q

Why is the spreading patten usually the same for a disease?

A
  • ARCHITECTURE of cell
  • ability of connected neurons to accept and propagate SEEDS
24
Q

What are the results when PD patients are given a graft of feotal neurons?

A
  • grafted neurons develop Lewy bodies
  • spreading process slow (11+ years)
25
Q

What was the key finding about neuron to neuron spread in the patient who had a tumour removed but then later got diagnosed with AD?

A
  • lesioned region had no tau aggregate pathology
  • SPACE/PROXIMITY affects aggregation/spread
26
Q

What are mechanisms for cell to cell transmission?

A
  • MVB fusion and exosomes (release)
  • exocytosis and endocytosis (release and uptake)
  • ectosomes
  • free translocation
  • nanotubes
27
Q

What is the mechanism for PrP (membrane protein) cell to cell transmission? What is important?

A
  • localization important
  • entry into cytoplasm is NOT required for PrP transmission
  • PrP has to contact normal PrPc on cells and then infect

(i.e. ENTRY INTO CELL NOT REQUIRED)

28
Q

TRUE or FALSE: the mouse study that looked at synuclein injection in the gut used SMALLER fibrils and much HIGHER amounts of fibrils, and they waited LONGER

A

TRUE

NEURO 411 (12 decks)

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