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Y3: PN3313 > Neurodegeneration > Flashcards

Neurodegeneration Flashcards

1
Q

what is neurodegeneration?

A

the progressive loss of neuronal structure, function and/or number

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2
Q

what is the overview of alzheimer progression?

A

healthy brain -> mild disease = shrinkage of cerebral cortex, enlargement of vesicles and hippocampal shrinkage –> severe disease= more drastic symptoms = amyloid plaques and disintegrating microtubules

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3
Q

what is the pathology of parkinsons?

A

diminished substantia nigra due to loss of neurons in the midbrain

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4
Q

what are 6 risk factors for neurodegeneration?

A 
age
genetics
lifestyle
head-heart
mild trauamtic brain injury
metabolic abberations
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5
Q

what are 5 cellular features of alzheimers disease?

A

amyloid plaques
accumulation of hyper phosphorylated tau protein
neuroinflammation
cell death

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6
Q

what are the 4 intracellular features of alzheimers?

A

intracellular amyloid accumulation
accumulation of hyper phosphorylated tau
mitochondrial dysfunction
oxidative stress

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7
Q

what is the pathology of alzheimers at an anatomical level

A

loss of cells in the cerebral cortex and hippocampus

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8
Q

what are three cellular features of parkinsons

A

accumulation of large bags of proteins= lewy bodies
neuro inflammation
cell death- substantia nigra

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9
Q

what are three intracellular features of parkinsons

A

alpha-synucleic aggregate in cells
mitochondrial dysfunction
oxidative stress and damage

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10
Q

what are the 6 stages of protein phosphorylation for neurodegeneration

A 
misfolding
dimers
olgimers
protofibrills
bigger aggregates / amyloid fibres
leading to toxicity neurodegeneration
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11
Q

what is tau

A

a microtubule associated protein

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12
Q

what are three advantages of microtubules in axons

A

neural outgrowth
axonal transport
microtubule dynamics

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13
Q

describe tau phosphorylation for physiological process

A

at sites serine 119/202 and threonine 205

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14
Q

what enzymes are thought to phosphorylate tau?

A

PKA and MARK

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15
Q

what happens when tau fillaments form?

A

no longer associated with microtubules

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16
Q

what are the phosphorylation sites in the pre tangles and neurofibrally tangles of AD

A

serine 62 and threonone 231

serine 442 in neuro tangles

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17
Q

what mediates serine 442 phosphorylation in AD

A

GSK-3beta

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18
Q

what is the leading cause of cell death in AD?

A

non functioning microtubules

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19
Q

what is the pathology of tau phosphorylation in AD?

A

tau filament formaiton
microtubule dysfunction
cell death

20
Q

what does abnormal phosphorylation lead to ?

A

hyperphosphorylation and a chain reaction

21
Q

What are the two pathways of proteolytic cleavage in AD?

A

non-amyloidogenic

amyloidogenic

22
Q

what is APP

A

amyloid precursor pathway

23
Q

what is the normal pathway for non-amyloidogenic pathway in AD?

A

chooping up soluble APP-alpha via alpha secretase
production of peptide p3
after these cuts- AICD left in membrane (maybe involved in signalling and axonal transport)

24
Q

what is the molecule involved in amyloidogenic pathway

A

soluble APP-beta and it is left in larger chunks when cut up so C99 left in membrane

25
Q

what is C99 left in the membrane in AD, further cleaved by

A

gamma secretase

26
Q

what produce amyloid beta

A

abnormalities of proteolytic cleavage of app, cleaved by non-amyloidogenic pathway
aggregate in and out of cell

27
Q

what can proteins aggregate by?

A

hyperphosphorylation

28
Q

what is a mechanism of alpha synucleic aggregation in parkinsons?

A

protein misfolding

cell under stress due to misfolding

29
Q

describe protein misfolding and parkinsons

A

need protein not just be long string of AA but fold so it can do its job - misfolded means cannot do job

30
Q

where are proteins folded?

A

in the ER and cytosol

31
Q

what happens to misfolded proteins?

A

protein intermediates can go to lysosome or others are broken down by ubiquitations or fold correctly in the cytosol

32
Q

what do misfolded proteins lead to in parkinsons

A

lewy bodies formation

33
Q

what are ROS

A

reactive oxygen species which are highly reactive and short lived

34
Q

what causes ROS

A

form of a free radical - unpaired electron

35
Q

describe ROS interaction with other molecules

A

interact by donating or recieving an electron to achieve stability

36
Q

what is an oxidative modification

A

addition of an oxygen molecule to or from a ROS

37
Q

what is oxidative stress

A

when production of ROS outweighs cells antioxidant defences leading to oxidative damage to nucleotides, proteins, and lipids

38
Q

what is one of the main cellular sources of ROS

A

mitochondria

39
Q

what is the vicious cycle between ROS and mitochondra

A

ROS causes damage leading to further production of ROS

40
Q

what are 4 genes associated with PD that affect mitochondria

A

SNCA
Parkin
Dj-1
LRRk2

41
Q

what are two molecules associated with mitcohdondrial dysfunction in the early stages of AD

A

APP or PSn1 mutations

42
Q

what are the 5 stages of microglia activation

A 
ramified (r-stage)
activation signal
transitional (t-stage)
motile (m-stage)
locomotory (l-stage)
43
Q

where can we find more microglia in AD patients

A

hippocampus and cortex

44
Q

where does stimulus for microglia come from in AD patients?

A

unknown damage signals- neuron damage activates microglia initiating an immune response

45
Q

describe microglia recruitmeent in PD

A

activation of death receptors

TNF alpha activates TNFR1 leading to cell death

Y3: PN3313 (23 decks)

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