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Senior seminar > Brain > Flashcards

Brain Flashcards

1
Q

Cytokines/cytotoxic mediators in the brain come from where?

A

Activated microglia can release them, (ROS and nitrogen species) –> apoptosis and loss of OL precurosors, dysregulation (failing to myelinate axons)

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2
Q

What is the knowledge gap

A

Molecular mechanisms eliciting inflammation thru placenta-fetal-brain axis are unknown

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3
Q

Rat brain is considered as developed as human newborn how many days postnatal

A

P10-12

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4
Q

Neurogenesis is what and starts when in rat vs human

A

rat: G0 - 10
human: 0 - 12 weeks
STEP 1: Neurogenesis: This is the earliest step, where neural stem cells in the ventricular zone differentiate into neurons.

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5
Q

Astrocyte and OLs start to generate after..

A

the beginnning of neurogenesis, and gliogenesi continues postnatally in both humans and rats

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6
Q

Astrogenesis is what step and what is it?

A

3RD STEP
following neurogenesis, radial glial cells differentiate into astrocytes, which support neurons and maintain the brain’s environment.

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7
Q

Microglial invasion is what step and what is it?

A

SECOND
Support immune protection and help shape developing neural circuits
Come from progenitor cells in the yolk sac
Start colonising the rat brain slightly after G10 continue to peak postnatally

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8
Q

What marks the 3rd trimester?

A

Beginning of synaptogenesis, astrogenesis, myelination (20-40 weeks human, G20-P12 rats)

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9
Q

When do OLs start developing ?

A

OLs start developing prenatally, maturating from pre-OLs to immature OLs from mid-gestation to the end of gestation

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10
Q

When does myelination occur?

A

prenatally and postnatally in humans but occurs postnatally in rodents

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11
Q

What is myelination and what step?

A

4th
Myelination: Oligodendrocytes wrap axons in myelin to speed up electrical signaling. In humans, myelination

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12
Q

What are the mechanisms linking maternal and fetal responses to brain damage?

A

Increased proinflammatory cytokines in the brain:
1) activated microglia (critical in synaptic plasticity/myelination)/astrocytes
- activation of these = neuronal migration processes, neuronal death, damage surrounding axons etc
2) maturation and death of OLs
3) axonal loss or death of neurons, cytoskeletal damage, neurotoxicity
Innate immune molecules may alter directly or indirectly some neuronal processes
Overall, cerebral dysconnectivity associated with hypomyelination

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13
Q

The nature and severity of brain injuries depend on…

A

The timing, intensity and nature of inflammatory insult

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14
Q

First trimester insults associated with?

A

brain maldevelopments

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15
Q

Second trimester insults associated with?

A

periventricular WM injury (periventricular leukomalacia)

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16
Q

Third trimester insults?

A

cortical and deep grey matter damage

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17
Q

Altered myelination is partially due to what?

A

impaired OL maturation

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18
Q

Effect of IL1b on brain?

A

ACTIVATE astrocyte and microglia cells
(and then these release more cytokines)
directly (i.e. by neurotoxicity) or indirectly (i.e. by modulating axonal guidance proteins and synaptogenesis) inhibit cell proliferation and neurogenesis, cause neuronal death, delayed myelination and disrupt neuroglial fibre tract growth and synaptic connections, which can lead to permanent alterations of brain connectivity

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19
Q

Pillars of ASD?

A
  1. repetitive/stereotype behavior
  2. impairments in communication / social behavior
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20
Q

ASD affects how many children?

A

1/60

21
Q

Among a cohort of ex-preterm ASD human subjects,

A
22
Q

Brain development in utero explain

A

Week 3 - ectoderm thickens and forms neural plate –> neural groove
Week 4 - neural tube, (become the brain and spinal cord)
Week 8 - most structures in place, wweek 11 - has a similar shape to what it will be like at birth

23
Q

Give examples of studies that have highlighted proinflammatory effect of androgen in the brain?

A

A study using finasteride (drug inhibits the formation of DHT) in a PPA-induced autism rat model. Neuroprotective effects, biochemical, histopathological, and behavioral analyses.

24
Q

What are OLs?

A

Glial cells that support and maintain integrity of axons and neuronal connectivity within the central nervous system

25
Q

Another study which shows protective effect of flutamide on OLs?

A

The study showed that flutamide prevented both the direct toxicity of testosterone and its ability to exacerbate excitotoxic damage induced by glutamate receptors in cultured oligodendrocytes

26
Q

Is there a conflict in the literature of T effects on the brain - neuroprotective/ neurotoxic?

A

Yes, some studies indicate that T low levels being protective and high levels being detrimental.

27
Q

In a study, blocking T conversion to estradiol did what?

A

Increased damage, estradiol as a neuroprotective factor against cerebral ischemia

28
Q

What happens to plasma levels of LH and T after acute flutamide tx?

A

Increase, reduces negative feedback on HPA

29
Q

In our study what is the effect of flutamide on hormonal balances?

A

More androgen = more conversion of A into E in brain tissue by aromatase

30
Q

How does estradiol regulate OLs?

A

E delays the exit of OPC from the cell cycle, so in our model the inc of CC1+ OLs may have resulted from estradiol prolonging the cell cycle of OPCs, thereby increasing the pool of mature OLs in flut/gbs group

31
Q

Why did GBS cause enlargement of LV?

A

Decrease of CC-1 oligodendrocytes in forebrain whtie matter = shrinkage of surrounding brain tissue due to a loss of mature OLs and subsequent demylination (Smaller bundles of axons and underdeveloped neuronal connections)

32
Q

What is often used to treat cerebral edema by reducing inflammation?

A

glucocorticoids (adverse effects like brain atrophy)

33
Q

What other effects on GBS could brain have?

A

Neuronal loss, cortical thickness,

34
Q

Is there evidence of androgen contributing to vulnerability in females and how?

A

Yes by androgenization of females

35
Q

Astrocytes in development ?

A

Derived from radial glial cells, beginning around E14 in rodents.

36
Q

Microglia in development?

A

Derived from yolk sac progenitors, migrating into the brain around E9

37
Q

OLs in development

A

Derived from oligodendrocyte precursor cells (OPCs), starting around E14 and maturing postnatally.

38
Q

Fronto-parietal tract

A

passes through EC
attention, working memory

39
Q

Thalamo-corticla tract

A

passes through EC
sensory integration and processing

40
Q

Amygdalo-hippocampal tract

A

passes through EC
social behaviors and emotion

41
Q

is iba-1 for activated microglia? explain more

A

activated - amoeboid shape, thicker retracted processes
M1 - proinflammatory -> proinflammatory cytokines, ROS
M2 - anti inflammatoyr (a bit less amoeboid than M1, more branches) -> BDNF, IL10, TGFb, clear debris wound healing

42
Q

why did cc-1 increase with flutamide?

A

LH and T plasma levels increase
flutamide, as an androgen receptor antagonist, reduces the negative feedback that testosterone and other androgens have on the hypothalamic-pituitary-gonadal axis
higher conversions of androgens into estrogens in brain tissues by aromatase
estradiol delays the exit of OPCs from the cell cycle
[37]. Thus, the observed increase in CC-1+ oligodendrocytes may result from estradiol’s role in prolonging the cell cycle of OPCs, thereby increasing the pool of mature oligodendrocytes in flutamide/GBS groups

43
Q

what about LV , why. did it increase

A

The observed decrease in CC-1+ oligodendrocytes in the forebrain white matter likely resulted in the observed enlargement of lateral ventricles in GBS-infected groups
This increase in size may reflect the atrophy or shrinkage of surrounding brain tissue due to a loss of mature oligodendrocytes and subsequent dysmyelination
likely be a result of the underdevelopment of neuronal connections, resulting in smaller bundles of axons within the forebrain white matter

44
Q

why was microglia not reduced in GBS induced ca?

A

previous studies in our lab noted a decreased in females in microglia but not males
in another stuyd, microglia depleted rats spent less time in open arms of EPM –> more anxiety, same as what our mdoel showed
GBS III showed dec microglia in CC
could have looked at microglial morphology, spacing, clustering as opposed to jsut density

45
Q

what else are microglia importnat in?

A

neuronal migration, prenatal brain circuit shaping, myelination, synpatogenesis
During neurogenesis, microglia influence the survival, differentiation, and apoptosis of neuronal precursor cells through the secretion of brain-derived neurotrophic factor and neurotoxic factors
In postnatal development, microglia facilitate synaptic formation and maturation via synaptic pruning
The involvement of microglia in long-term synaptic plasticity serves as the foundation for learning and memory processes

46
Q

which cell type produces myelin

A

schwann cell

47
Q

why arent microglia activated in our model?

A

Time point matters - this is at P50, microglia could have already turned to a less active state, we could have missed earlier peaks

48
Q

how can il1b inhibit neurogenesis

A

Directly: By damaging neurons through its toxic effects.
Indirectly: By disrupting critical developmental processes like axon growth and synapse formation.

49
Q
A

Senior seminar (9 decks)

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