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1
Q

why is neuron regeneration different from other cells?

A

nervous tissue does not do mitosis.

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2
Q

what is happening in the brain when functionally recovering from a stroke?

A

when one area is diminished, there can increased activity in other areas compensating for the damaged area.

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3
Q

3 types of neuronal repair

A
  1. axon regrowth
  2. neuronal regrowth (in PNs not CNS
  3. stem cell repair. happens only in specific regions (hippocampus and olfactory)
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4
Q

Henry Head

A

cut his own radial nerve and monitered recovery of sensation over time.

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5
Q

4 major cellular elements of nerve repair

A
  1. schwann cells
  2. fibroblasts
  3. macrophages
  4. endothelial cells
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6
Q

what happens when a peripheral nerve is cut?

A

axon degenerates starting with the distal end. macrophages move in to clear out myelin debris.
Schwann cells stop making myelin and secrete growth molecules like NGF as well as form tracks to aid axon growth.
schwann cells provide scaffolding for the now formed growth cones
remyelination.

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7
Q

molecular signals for repair

A
  1. downregulation of factors during demyelination. (maintenance genes turning off to make room for development; Wnt)
  2. factors expressed during the repair program. (development genes like notch)
  3. factors involved during remyelination
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8
Q

how can you artificially aid regeneration?

A

artificial biomaterial can serve as a scaffold for nerve bridges and acetylcholine receptors will remain around the dead synapse so it will be functional.

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9
Q

why are central neurons limited in regeneration

A

damage to central neurons activates necrotic and apoptotic cell death mechanisms.
changes at the site of injury do not produce the developmental signals or environment for growth

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10
Q

what is the purpose of the blood brain barrier

A

it allows for tight regluation of ions, molecules, and cells between the blood and the brain. it protects the brain from toxins and pathogens.

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11
Q

layers/things that protect the brain

A

skill, dura matter, arachnoid matter, pia matter (blood vessels), and spinal fluid. and the blood brain barrier

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12
Q

chronic traumatic encephalopathy

A

getting head knocked around by acceleration changes, blast injuries, or direct brain injuries is bad. repeated concussions increases likelihood of CTE. results in personality changes and Alzheimer’s symptoms. can be mistaken for alzheimers but differentiated by neuronal tangles.

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13
Q

symptoms of a concussion

A

headache, memory deficits, nausea, mood changes, and cognitive impairment.

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14
Q

what is the central neuron response to hypoxia

A

activation of transcription and apoptotic signaling cascade. process takes about 24 hours.

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15
Q

what does a glial scar do

A

isolates injury site to prevent damage spread but also opposes regrowth

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16
Q

how the glial scar forms

A

microglia transition to their phagocytic state.
astrocytes develop into activated astrocytes (support recovery) and scarring astrocytes (form tissue around injury, scar)
immune cells enter and interact with glial cells.

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17
Q

how do glial scars prevent regrowth

A

they have or secrete inhibitory signals and newlt generated or cut axons express receptors for them.

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18
Q

carbon 14 study for neurogenesis in the CNS

A

carbon 14 put in atmosphere from nukes, studied people born between 1933 and 1973. if they were making neurons carbon 14 would have incorporated into their DNA, there was none found

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19
Q

mammalian CNS neurogenesis

A

subgranular zone near hippocampus and olfactory neurons continuously regenerate.

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20
Q

calcium and glutamate excitotoxicity as a type of non apoptotic cell death mechanism: setup

A

during a stroke there is no oxygen so no ATP production leading to no maintenance of membrane potentials. neurons depolarize and release neurotransmitter (glutamate).

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21
Q

calcium and glutamate excitotoxicity as a type of non apoptotic cell death mechanism: glutamate and calcium toxicity

A

NMDA receptor is depolarized and glutamate has been released and has bound. channel opens and calcium flows into the cell. activates enzymes and depolarized mitochondria resulting in apoptotic factors being released.

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22
Q

prevelance of N2B subunit

A

subunit on NMDA receptors involved in neurodegeneration.

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23
Q

calcium and glutamate excitotoxicity as a type of non apoptotic cell death mechanism: spillover

A

excess glutamate can not be cleaned up fast enough and activates extrasynaptic NMDA receptors.

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24
Q

mitochondria in excitotoxicity: how calcium results in apoptosis

A

excess calcium in the cell moves into the mitochondria through the calcium uniporter. membrane depolarizes and increased reactive oxygen species are released. ROS are also released and can damage DNA and proteins.

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25
zinc in excitotoxicity
zinc is released with glutamate and enters cells via calcium pathways. can enter mitochondria and effects things similarly to calcium.
26
autophagy in non apoptotic cell death
this is the recycling mechanism in cells, it can be disrupted and toxic things will build up in the cell
27
autophagy in non apoptotic cell death: macro autophagy and related disorders
phagophore forms around proteins and engulfs them as it becomes an autophagosome. proteins get broken up. disruptions in the autophagosome are implicated in parkinsons and huntingtons.
28
autophagy in non apoptotic cell death: mitophagy mechanism
mechanism to get rid of dysfunctional mitochondria. PINK1 accumulates on depolarized mitochondria, PINK1 recruits parkin and signals for autophagosomes to degrade the mitochondria. mutated PINK1 results in early onset parkinsons.
29
signs of stroke
numbness/wekness on one side (contralateral), trouble walking, confusion with speech, and trouble seeing.
30
risk factors of stroke
age, sex, stroke history, genetics.
31
ischemia
inturuption of blood supply
32
what is a stroke
acute rapid onset vascular event that results in destruction of a region of the brain.
33
anoxia
reduced blood supply that deprives tissue of oxygen and glucose and prevents removal of toxic metabolites
34
infarction
structural damage to neurons from stroke
35
ischemic stroke
blood clot stops flow of blood to the brain
36
hemorrhagic stroke
blood vessel rupture in the brain
37
necrotic core and penumbra
in the necrotic core, cells immediately die. in the penumbra neurons are depolarized and not functional. over time the necrotic core grows and the penumbra shrinks.
38
what mechanism is responsible for the effect of a stroke
excitotoxicity, cell death signalling, blood brain barrier breakdown, and ROS production are all implicated. excitotoxicity followed by oxidative stress, then inflammation and brekdown of blood brain barrier, and finally apoptosis.
39
stroke treatment
we need a drug that can target N2B subunit NMDA recptors which cause activation of cell death proteins, but we dont have one. there is a critical window for stroke treatment, clot dissolvers and mechanical clot removal is used. drugs are aimed at freezing the penumbra and stem cells show promise.
40
working memory
Seconds to minutes. E.g. while searching for a lost object. Cognitive dysfunction associated with STM deficits.
41
working memory vs declarative memory
work on different systems in the brain. when comparing patients with selective damage to different brain areas, one area produced poor declarative, the other produced poor working memory.
42
what is involved in consolidation
involves changes in gene expression likely linked to long term changes in synaptic transmission or growth and reordering of synaptic connections.
43
declarative memory
explicit, available to consiousness. for example, words and their meanings, history, daily episodes.
44
nondeclarative memories
implicit, generally not available to consiousness. for example, motor skills, priming cues, puzzle solving skills, and association.
45
priming
a change in the processing of a stimulus due to a previous encounter with the same or related stimulus with or without conscious awareness of the original encounter. not always reliable but resistant to aging and dementia.
46
ventral tegmental area znd reward learning
large awards activate the ventral tegmental area which leads to greater activation in the hippocampus. a greater reward leads to a greater dopamikne response and better memory associated.
47
hippocampus in declarative memory
hippocampal lesions result in not remembering. H.M. had parts of hippocampus removed for seizures, resulted in 50 first dates scenario.
48
where are long term memories stored
hippocampus projects into wide regions of the cerebral cortex. declarative memories are stored in specialized areas for processing like the visual cortex.
49
3 stages of alzheimers
mild: memory loss, speech deficits, mood changes moderate: learning impairment, agression, dementia severe: bedridden, motor impairment.
50
what is alzhemers characterized by
presence of neurofibrillary tangles, plaques, and diffuse neural cell death. shrinkage in hippocampus.
51
plaques vs tangles
plaques are extracekkukar, tangles are inside.
52
amyloid hypothesis
altered genes in those with familial alzheimers promote aggregation of B-amyloid. increased production ir decreased removal of amyloid is thiught to be a central event and the appearance of B-amyloids in blood is an early biomarker. AB is derrived from APP, APP is activated by secretases. products are usually soluble and found in blood. AB can activate NMDA receptors and cause excitotoxicity.
53
tau hypothesis
Tau usually stabalizes microtubules, but can undergo phosphorylation that will result in it aggregating into tangles that are bad for neurons
54
AB and Tau: 3 mechanisms they could be working together in
1. AB causes hyperphosphorylation of tau 2. AB is the toxic agent but is mediated by tau 3. tau and AB on mitochondria produces toxicity
55
tau and mitochondrial trafficking
increased phosphorylated tau effect microtubules so you dont get mitochondrial trafficking. AB enters mitochondria through TOM complex.
56
3 component of emotions
behavioural manifestations, a subjective feeling, a physiological state
57
2 systems of the nervous system that organize expression
volitional movement like voluntary facial paresis (motor cortex and brainstem) and emotional expression like emotional facial paresis (medial forebrain and hypothalamus). there are 2 different muscle pathways
58
amygdala
fear recognition centre. prefrontal cortex sends processed senory experiences to the amygdala.
59
fear conditioning
model of associative learning in the amygdala relevant to emotional function. Pairs a stimulus with an aversive stimulus, learns fear. Relies on strengthening synapses. LTP is involved.
60
environmental factors in parkinsons
herbicides and pesticides increase risk, more prevelant in rural areas. dairy and ciggarettes lower risk.
61
MPTP
MPTP made by a kid who was trying to make MPPP a synthetic opiod, upon injecting he got immediate parkinsons symptoms. MPTP dissociates into MPP+ and gets taken through the dopamine system and destroys dopaminergic neurons.
62
pathophysiology of parkinsons
A disease of dopamine disruption which disrupts behaviour and cognition, working memory and learning, and coordinated muscle movement. Characterized by lewy bodies made up of alpha synuclein. You have to get down to 50% dopaminergic neurons lost to get to a diagnosis point. no myelinated neurons in the substantia nigra.
63
lewy bodies
made up of alpha synuclein. malfunctioning a-synuclein prevents formation of dopamine transport vesicles. dopamine metabolism releases ROS and with excess dopamine excess ROS increases. evidence a-sybuclein works in a prion fashion.
64
Parkin in parkinsons
parkin tags mitochondria for degradation, mutation in parkin means early onset parkinsons.
65
levodopa
parkinsons treatment that is a dopamine precurosor making it easier for remaining dopaminergic neurons to make and move dopamine.
66
mechanism for ALS
neuroinflammation, mitochondrial dysfunction, excitotoxicitym and glial dysfunction. mutated SOD1 protein.
67
multiple sclerosis
neurological demyelinating disease characterized by inflammation mediated focal demyelination.
68
types (progression) of MS
Clinically isolated syndrome- one instance, earliest forms Relapsing-remitting MS- attacks, 80% of patients, during relapses new symptoms can appear or existing iones can get worse Secondary progressive MS- 10 years after initial symptoms. Increasing diability, no attacks and remissions. Primary progressive MS- slow insidious progression.
69
MS lesions
where the immune system is attacking the myelination.
70
3 types of cortical lesions in MS
(a) Type I lesions affect both white and gray matter. (b) Type II lesions are small perivascular areas of demyelination. (c) Type III lesions extend from the pial surface into the cortex and often demyelinate multiple gyri.
71
3 Different types of injuries in the CNS
1. Traumatic brain injury. 2. Local oxygen deprivation (Hypoxia/Stroke). 3. Neurodegenerative diseases.
72
what differences are there in the brain between CTE and alzhemers
CTE has astrocytic tangles and alzhemiers does not. CTE has tau and astocytic tangles in the perivascular area but in alzhemers tau tangles are elsewhere.
73

bisc 405 (4 decks)

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