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BCS 246 Bio of Mental Disorders > Exam #2 > Flashcards

Exam #2 Flashcards

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Biology 101 flashcards
1
Q

What does SNR stand for?

A

Substantia nigra pars reticulata-works with GPi

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2
Q

What does SNc stand for?

A

Substantia nigra pars compacta

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3
Q

What does STN stand for?

A

Sub thalamic nucleus-modulator of basal ganglia output

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4
Q

Apoptosis

A

Programmed cell death

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5
Q

What can the Wt protein do that the mutant protein (expanded form) can’t do?

A

Prevent apoptosis, prevent excitotoxicity, regulate gene transcription, axonal transport, mitochondrial health

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6
Q

Why is there more apoptosis in mutant protein?

A

More PolyQ, leads to more caspase-9= “excecutioners”, expanded cells more susceptible to apoptosis

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7
Q

Autophagy

A

Process of aberrant (not normal) organelles breakdown inside autolysosome (isolation membrane–>autophagosome–>lysosome)

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8
Q

Mitophagy

A

Breakdown of mitochondria

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9
Q

What happens if lysosomal autophagy is disrupted?

A

Dysfunction and deregulation

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10
Q

Aggregation

A

Formation of a number of things that form a cluster

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11
Q

Aggregation in HD

A

Caspase-6 site-generates N-terminal fragments (PolyQ) that aggregate in cytoplasm and nucleus (GAIN OF FUNCTION), intracellular

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12
Q

Aggregation in AD

A

Amyloid forms aggregates extracellularly–> amyloid plaques

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13
Q

Aggregation in PD (4)

A
  • Alpha-syn. (found in Lewy bodies) forms aggregates
  • WT, A30P, & A53T form lipid-based aggregates
  • Dysfunction of ubiquitin proteasome system and lysosomal autophagy leads to failure to remove aggregates
  • Beta sheets are bad: sticky–>aggregates
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14
Q

Excitotoxicity

A

Process by which nerve cells are damaged or killed by excessive stimulation by NTs, such as glutamate

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15
Q

What does excitotoxicity lead to?

A

Depolarized cell: impaired mitochondrial membrane potential–> more Calcium–> reduced ATP/ADT ration and increased NMDA currents (mimics glutamate)

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16
Q

Excitotoxicity in AD

A

Amyloid beta (plaques) activate astrocytes and microglia–> secretion of toxic cytokines

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17
Q

How does normal Whtt protein protect against apoptosis and caspase activation?

A
  • BCL2 is protective of mitochondria from apoptosis
  • Does not have more caspase-9 like mutant htt
  • Not as susceptible to NMDA toxicity
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18
Q

Symptoms of HD and why

A

Chorea (violent jerking movements) because of the disease favoring direct pathway. Indirect pathway neurons are most affected, which usually prevents unwanted movement

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19
Q

Symptoms of AD and why

A

Decline in memory because of loss of cortex and hippocampus (large pyramidal cells most vulnerable), neuronal death (apoptosis, excitotoxicity, mitochondrial dysfunction, calcium dynamics, inflammation), plaques and tangles

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20
Q

Symptoms of PD and why

A

Resting tremor, rigidity, bradykinesia (slowed movement) or akinesia (lack of movement), postural instability because of loss of DA and SN neurons, DA deficiency in striatum
-Favors indirect pathway

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21
Q

Mixed diseases (2)

A

Dementia with Lewy bodies and HD

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22
Q

What causes plaques in AD?

A

Aggregation of Amyloid Beta

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23
Q

What causes tangles in AD?

A

Taupathy: binds well to itself, rather than microtubules

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24
Q

What causes tangles in AD?

A

Taupathy: binds well to itself, rather than microtubules

-Hyperphosphorylation of Tau

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25
Q

Genetic causes of HD

A

Autosomal dominant, 50/50 chance, caused by mutation in Htt gene, >37 CAG repeats

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26
Q

Genetic causes of AD

A

Autosomal dominant,

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27
Q

Genetic causes of AD

A

Idiopathic (arises from itself), only 5% genetic, APOE4 allele is a risk factor

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28
Q

What 3 genes do autosomal dominant genes express in AD?

A
  1. APP
  2. Presenilin 1
  3. Presenilin 2
    (2&3 make up gamma secretase)
    All affect amount of Ab42
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29
Q

Genetic causes of PD

A

Alpha-syn. mutation or overexpression, DJ-1, Parkin, PINK-1, LRRK-2
-mutation on chromosome 4 at SCNA gene that codes for alpha-syn.

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30
Q

Environmental causes/risks in HD

A

Environment has no role in creating or decreases risk, genotype=phenotype in HD

31
Q

Environmental causes/risks in AD

A

None specifically mentioned, higher education level and more exercise could be protective factor

32
Q

Environmental causes/risks in PD

A

Exposure to herbicides/pesticides (inhibits complex 1), living in rural environment, consumption of well water, proximity to industrial plants or quarries, metal exposure, PCBs
-Smoking/caffeine associated with lower risk

33
Q

What does it mean to have a mutation in APP?

A

Causes increased amounts of Ab–>plaques, leads to familiar AD, just mutating APP doesn’t do much-have to wait a few years to see anything

34
Q

What does it mean to have a mutation in alpha-syn?

A

Genetic risk factor in PD, linked to familiar PD

35
Q

What does it mean to have a mutation in GBA?

A

Increases risk of familiar and sporadic PD, reduces PD age-of-onset and increases cognitive decline

36
Q

What does it mean to have a mutation in APOE?

A

Possibly halts AD? APOE4 is bad, APOE2 is a protective factor against AD

37
Q

Treatments for HD

A

No treatment to stop or reverse HD :(

-possibly could use tetrabenazine (prevents DA from entering vesicles, can’t be released)

38
Q

Treatments for AD

A

Cholinesterase inhibitors: slows breakdown of Ach by blocking the activity of acetylcholinesterase

39
Q

Treatments for PD

A

Levadopa, etc. (not really talked about in lecture but on slide)
-Apomorphine, dual pump, adenosine A2A receptor agonist, inosine, nilotinib, anti alpha-syn. antibodies

40
Q

Treating symptoms vs disease in HD

A

None for either, possibly tetrabenazine for symptoms, exercise helps

41
Q

Treating symptoms vs disease in AD

A

Cholinesterase inhibitors for symptoms, can’t cure AD

42
Q

Treating symptoms vs disease in PD

A

No cure for disease, can use deep-brain stimulation to STN or GPi to relieve symptoms (goal is to block overactivation of GPi/SNr)

43
Q

What type of system was used in hREST study?

A

Conditional expression system to overexpress hREST first in neural stem cells and later in striatal neurons that express the D2 receptor

44
Q

Why use conditional expression system in hREST study?

A

Constitutive REST overexpression model in mice is embryonically lethal

45
Q

Why are dopamine neurons more susceptible to MPTP?

A

MPP+ looks like DA, MPTP selectively targets DA in SN and inhibits complex 1 of mitochondria

46
Q

Evidence that there is decline in NGF transport with age in cholinergic neurons?

A

Decrease in NGF and TRKA receptor leads to increase in p75NTR which is linked to cell death, can also lead to increase in Ab
-decreased NGF receptors

47
Q

What causes expansion in HD?

A

Slippage in DNA polymerase

48
Q

Anticipation (HD)

A

Age of onset appears earlier (symptoms more severe too) as the disorder is passed from one generation to the next

49
Q

Gain of function features in Htt gene

A

Expanded polyQ enables protein to do something it normally couldn’t do

50
Q

Loss of function features in Htt gene

A

PolyQ prevents protein from doing what it normally does

51
Q

Cholinergic Hypothesis

A
  • Inability to obtain or use NGF underlies demise of CBF neurons
  • Basil forebrain cholinergic (CBF) cell death correlates with disease severity, pathology, and synapse loss
  • In AD
52
Q

What is APP good for? (4)

A
  1. Axonal transport
  2. Cell adhesion
  3. Cell growth
  4. Synaptic plasticity
53
Q

BACE inhibitor

A

Beta secretase inhibitor, reduces Ab production, KO has rescued memory defect in mice, in AD

54
Q

HDAC inhibitor

A

Preserves learning and memory performance in mice, restores “lost” memory in mice

55
Q

Synaptic NMDR

A

Activates CREB, stimulates BDNF, neuroprotective, more alpha-sec., less Ab

56
Q

Extrasynaptic NMDR

A

Decreased CREB, BDFN, dysregulate mitochondria, glutamate toxicity, less a-sec., increased Ab, increased BACE

57
Q

Where does glutamate enter in synaptic NMDR?

A

Glut released from vesicles

58
Q

Where does glutamate enter in extrasynaptic NMDR?

A

Activated by spillover glutamate at dendrite shaft, cell body

59
Q

Memantine/nitromemantine

A

Targets extrasynaptic NMDARs, decreased Ab levels

60
Q

Does Ab stimulate glutamate release and where? Synaptic or extrasynaptic?

A

Engages alpha-7 nicotinic acetylcholine receptors to release astrocytic glutamate–>extrasynaptic NMDA receptors on neurons

61
Q

What happens in post-synaptic neurons after glutamate is released?

A

Increases in calcium and nitric oxide, chronic Ab exposure in-vivo shows increased glu baseline current

62
Q

Does Abeta affect synaptic plasticity?

A

In hippocampus, eNMDAR activity is followed by reduction in evoked and miniature EPSCs

63
Q

What happens in spines after Ab activation of eNDMAR?

A

Greater presence of phosphorylated Tau, in-vivo synapse loss

64
Q

What gene does REST target?

A

DRD2, strong binding in striatal neurons

65
Q

Apomorphine (APO)

A

Dopamine receptor agonist that rescues loss of DA due to MPTP

66
Q

Point mutations causing accelerated aggregation of alpha-syn? (2)

A

A53T (more potent), A30P

67
Q

What do PINK1 and Parkin do?

A

Work together to induce mitophagy, mutations here cause issues

68
Q

What does LRRK2 do?

A

Important for synaptic vesicle formation, KO’s have fewer and smaller vesicle size with altered vesicular recycling

69
Q

How does L-DOPA work?

A

Prevents metabolism outside of the brain and increases efficiency/availability of L-DOPA crossing BBB

70
Q

Neuroprotective factors in PD (3)

A
  1. Nicotine
  2. BDNF treatment
  3. Exercise
71
Q

Do gut microbiomes effect locomotor behavior?

A

Alpha-syn. overexpression (ASO) without gut bacteria (GF), short-chain fatty acids seem to “mediate” PD gut-brain signaling

72
Q

What is the effect of gut microbiome on alpha-syn. pathology?

A

GF-ASO mice microglia look like Wt

73
Q

Are effects of gut microbiome something determined early in life or is it an active, lifelong communication?

A

Active, lifelong communication

BCS 246 Bio of Mental Disorders (1 decks)

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