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NSCI 4501 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

primary motor symptoms of PD

A
  • bradykinesia: slowness and lack movement
  • tremor at rest
  • rigidity
  • flexed posture and postural instability
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2
Q

cardinal feature of PD

A

bradykinesia

almost all have

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3
Q

secondary motor symptoms of PD

A
  • freezing of gait
  • micrographia
  • mask-like expression
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4
Q

why do PD patients have micrographia

A

difficult to concetrate on the size of the writing and the thing they are writing

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5
Q

non motor features of PD

A
  • sleep disorders
  • autonomic function
  • sensation loss
  • cognitive impairment
  • mood
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6
Q

autonomic function problems in PD are likely due to

A

denervation

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7
Q

main neuropathological hallmarks of PD

A
  • loss of dopamenergic neurons in the SNpc
  • loss of pigmented neurons in the SNpc
  • lewy bodies
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8
Q

The motor symptoms of PD result from the loss of which neurotransmitter?

A

dopamine

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9
Q

Which neurons are most severely lost in PD patients?

A

Neurons in the Substantia nigra Pars Compacta

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10
Q

if dopamine is lost in PD, why do treatments use L-Dopa?

A
  • dopamine is too big to cross the BBB
  • dopamine broken down too quickly
  • L-Dopa does not do these things
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11
Q

therapeutic targets to improve dopamine neurotransmission in PD

A
  • viral expression of tyrosine hydroxylase (makes L-Dopa)
  • expression of AADC (makes dopamine)
  • MAO/COMT inhibitors
  • DAT inhibitors
  • DA receptor agonists
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12
Q

MAO/COMT does what

A

breaks down dopamine

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13
Q

PD treatment by using DA receptor agonists helps because

A

dopamine is relased more since the receptors don’t signal that it is not needed anymore

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14
Q

PD treatment by using DAT inhibitors helps because

A

DAT not there to uptake dopamine

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15
Q

critical advancements in discovering PD

A
  • DA recognized as a neurotransmitter
  • MPTP usage by addicts causing parkinson’s like symptoms
  • genetic causes discovery
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16
Q

MPTP is

A

a prototypical DAergic toxin
* causes degeneration of DAergic neurons

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17
Q

how does MPTP cause loss of DA neurons

A
  1. MPTP crosses BBB
  2. MPTP turned into MPP+ by MOA-B in astrocytes
  3. MPP is uptaked via DAT into mitochondria
  4. oxygen free redicals and energetic failure in mitchondria = cell death
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18
Q

current therapies for basal ganglia circuit in PD

A
  • DA or cell therapy replacement
  • surgical pallidotomy
  • DBS
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19
Q

Deep brain stimulation treats the motor symptoms of Parkinson’s Disease patients by:

A

interfering with signals in the basal ganglia circuit in the brain

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20
Q

PD has loss of D1 or D2 neurons

A

D1

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21
Q

Mutations in which of the following genes is not considered a monogenic cause of PD?

SNCA
PINK1
GBA
LRRK2

A

GBA

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22
Q

Which genetic mutations is the most common cause of PD?

IMPORTANT - MIGHT BE ON EXAM

A

LRRK2

IMPORTANT - MIGHT BE ON EXAM

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22
Q

Which genetic mutations is the most common cause of PD?

IMPORTANT - MIGHT BE ON EXAM

A

LRRK2

IMPORTANT - MIGHT BE ON EXAM

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23
Q

According to Braak, where does alpha-synuclein pathology (Lewy Bodies) first appear in the CNS of PD cases?

A

Dorsal Motor Nucleus of Vagus

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24
Q

10% of PD cases are

A

genetic

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25
Q

Parkin mutations are _ _

A

autosomal dominant

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26
Q

genes involved in PD that mutate

A
  • SNCA
  • PINK1
  • DJ-1
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27
Q

parkin is a _ that is important in _

A

E3 ligase important for Ub tagged degredation

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28
Q

PINK1 mutations are

A

autosomal recessive

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29
Q

PINK1 normally has a _ and function to _

A

mitochondrial targetting motif and localizes to mitochondria

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30
Q

PINK1 regulates

A

mitochondrial fussion/fission

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31
Q

in animals, deletion of PINK1 led to

A

muscle atrophy

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32
Q

in animals, deletion of PINK1 was corrected by

A

overexpression of Parkin

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33
Q

PINK1 normally _ parkin

A

recruits and activates parkin

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34
Q

parkin/pink 1 mutations have:
* onset
* symptoms
* degeneration
* pathologies

A
  • onset before 40
  • slow or no symptoms
  • selective degeneration of SNpc and locus coeruleus neurons
  • no lewy bodies or tau pathologies
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35
Q

Parkin/PINK1 knockout mice features

A
  • no neurodegeneration
  • loss of DA neurons sometimes
  • no increase of vunerability of DA neurons ot MPTP or synuclein toxicity
  • overexpression of parkin protexted DA neurons from MPTP and alpha synuclein toxicity
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36
Q

overexpression of parkin…

A

protected DA neurons from MPTP and alpha synuclein toxicity

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37
Q

DJ-1 is what type of mutation

A

point mutation

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38
Q

L166P mutant is in what gene

A

DJ-1

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39
Q

DJ-1 knockout mice have severe or mild phenotype

A

mild

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40
Q

SNCA mutations are _ _

A

autosomal dominant

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41
Q

synuclein normally functions

A

as a synaptic chaperone
* important to inhibition of vesicle release (inhibit neurotransmitter release)

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42
Q

alpha synuclein antibodies…

A

recognize lewy bodies

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43
Q

lewy bodies are composed of

A

fibrillar alpha synuclein

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44
Q

alpha synuclein aggregates form

A

lewy bodies

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45
Q

two other types of alpha synucleinpathies

A
  • dementia with lewy bodies
  • multiple system atrophy (MSA)
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46
Q

what parts of the brain show Lewy Bodies in PD

A

Hippocampus
Locus Coeruleus
Vagal Nerve

IMPORTANT

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47
Q

Toxic conversion of alpha-synuclein is thought to involve:

A

formation of beta sheet structures

IMPORTANT

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48
Q

Which of the following are genetic risk factors for sporadic PD?

APP
PINK1
Parkin
MAPT

A

MAPT

IMPORTANT

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49
Q

synucleins inhibit

A

neurotransmitter release

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50
Q

alpha synuclein antibodies recognize

A

lewy bodies, lew neurites and GCIs

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51
Q

in SMA and dementia in lewy bodies, alpha synucleinopathies occur in

A

oligodendricytes

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52
Q

in SMA and dementia in lewy bodies, alpha synucleinopathies occur in

A

oligodendricytes

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53
Q

alpha synuclein pathology in PD initiates from _ and moves _

A

the brainstem and moves anteriorally

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54
Q

expression of A53T Hu alpha syn leads to

A

fatal neurological disease in Tg mice

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55
Q

human alpha synuclein transgenic mice features

A
  1. sudden onset
  2. rapid progession
  3. within 10 days, catatonic
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56
Q

expression of A53T Hu alpha syn

A

causes neurodegeneration in DA neurons

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57
Q

LRRK2 is important to

A

innate immunity
membrane trafficking
other things

gene important in PD

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57
Q

LRRK2 is important to

A

innate immunity
membrane trafficking
other things

gene important in PD

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58
Q

homzygous loss of function in _ causes Gaucher disease

A

GBS

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59
Q

LRRK2 pathology

A
  • lewy bodies
  • alpha syn aggregates
  • extran SN degeneration
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60
Q

LRRK2 mutation are _ inheritance

A

autosomal dominant

PD

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61
Q

LRRK2 mutation PD has clinical pathology

A
  • progressive
  • common non motor abnormalities
  • dementia
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62
Q

PRKN PINK 1 and DJ1 inheritance

A

autosomal recessive

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63
Q

PRKN PINK DJ 1 mutations pathologies

A
  • no lewy bodies
  • selective SNpc degeneration
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64
Q

clinical PRKN PINK1 DJ1

A
  • slowly progressive
  • limited non motoric abnormalities
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65
Q

lack of GBA causes dysfunction in

A

the lysosomes

PD

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66
Q

lack of GBA causes dysfunction in

A

the lysosomes

PD

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67
Q

genes that are heriditary PD

A
  • LRRK2
  • PRKN
  • PINK1
  • DJ-1
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68
Q

genes that are sporadic PD risk

A
  • SNCA
  • GBA
69
Q

pathology of sporadic PD

A
  • lewy bodies
  • alpha syn aggregates
  • SNpc and SN degeneration
70
Q

clinical features of sporadic PD

A
  • progressive
  • common non motoric abnormalities
  • dementia
71
Q

targets for PD treatment

A
  • alpha syn aggregates
  • targets of alpha syn aggregates
72
Q

many clinical defects of PD do not respond to

A

DA replacement therapy

73
Q

LRRK2 mutation increases

A

alpha syn in glia (astrocytes, microglia)

74
Q

if PD starts in the gut, alpha syn is carried ot the brain via

A

vagal nerve

75
Q

a vagotomy _ in PD

A

decreases the risk of developing PD

76
Q

injection of al[ha syn in the gut in animal models let to _ unless

A

led to alpha syn in the brain unless the vagal nerve was cut

77
Q

CNS pathology after initiation of alpha syn in the gut is first seen in _ and leads to

A

DMV, leads to progressive loss of SNpc DA neurons

PD

78
Q

alpha syn pathology in the ER

A
  • ERAD defect
  • ER caspase 9 and 3 activation
    **lack of P-eIF2a activation
    **
79
Q

P-eIF2a activation is important for

A

protecting the ER from stress

PD

80
Q

salubrinal

A

inhibits dephosphorylation of P-eIF2a
* protects cells from ER stress

81
Q

ER derived alpha syn oligomers are

A
  • highly pathogenic in animal models (very toxic)
82
Q

a syn pathology activatives c-Abl which leads to

A

impairment of p53 dependent autophagy by inhibiting Mdm2

83
Q

nilotinib

A

treatment that inhibits c-Abl so inhibits the inhibition of p53
* works to help a little in animal models

PD

84
Q

nilotinib

A

treatment that inhibits c-Abl so inhibits the inhibition of p53
* works to help a little in animal models

PD

85
Q

prion diseases can be

A
  • aquired
  • genetic
  • sporadic
86
Q

prion diseases manifest as

A

rapid progressive demtias with clinical visual or cerebellar signs and mutism

87
Q

sporadic, iatrogenic and familial CJD symptoms

A

progressive dementia and neurological signs

88
Q

variant CJD symptoms

A

early psychiatric symptoms, neurological deficits and cognitive decline

89
Q

GSS symptoms

A

cerebellar dysfunction

90
Q

pathological characteristics of prion diseases

A
  • brain vacuolation (holes)
  • astrogliosis
  • neuronal cell death
  • PrP amyloid plaques
91
Q

general structure of prion

A
  • 2 charged clusters
  • octapeptide repeat protein
  • hydrophobic domain
  • glycosylations
  • protein with GPI anchor
92
Q

prion cleavage sites and when

A
  • alpha - occurs normally
  • beta and gamma - occurs during stress
93
Q

sCJD has _ PrP plaques

A

little to none

94
Q

kuru has _ Prp plaques

A

some/medium

95
Q

vCJD has _ PrP amyloid plaques

A

a lot

96
Q

list the types of CJD with little to alot plaques in order

A

sCJD, kuru, vCJD

97
Q

prion strains affect/are different in

A
  • shape of aggregates
  • what brain regions they’re in
  • what disease they’re involved in
98
Q

prion strains affect/are different in

A
  • shape of aggregates
  • what brain regions they’re in
  • what disease they’re involved in
99
Q

sCJD has _ prion strains

A

no coexisting prion strains

100
Q

sCJD has _ prion strains

A

coexisting prion strains

101
Q

vCJD has _ prion strains

A

coexisting

102
Q

statistics of prion diseases

A
  • rare
  • older incidence
  • white people
103
Q

entry sites of acquired prion diseases

A
  • intracranial
  • coreal
  • airway
  • ingestion
  • intramuscular
  • intravenous
104
Q

the passage of prions from one species of the other is _

A

inefficient

105
Q

species barrier

A

prion diseases dont pass easily between species, absolute or partial transmitssion

106
Q

models for the confirmational conversion of PrPc into PrPsc

A
  • template directed refolding
  • seed nucleation
107
Q

early change in PrP toxicity

A

removal of synapses

108
Q

PrP overexpressing transgenic mice features

A
  • neuronal loss
  • PrP Sc deposits
  • Gliosis
  • Premature death
109
Q

in Prion diseases, see _ in MRI DWI

A

cortical ribbons

110
Q

PSWC in Prion diseases shows

A

??

EEG

111
Q

biomarkers in CSF in prion diseases

A
  • 14-3-3
  • Tau
112
Q

CUrrent strategies of treatment of prion diseases

A
  • Prnp knockdown (prion production)
  • antibodies to prevent prion conversion
  • antibodies to prevent prion aggregation
  • compounds to interfere with neurotoxicity
113
Q

the primary determinants of TSEs are

A
  • primary sequence of PrPc
  • route of entry of PrP Sc
114
Q

_ are good noninvasive biomarkers of prion diseases

A
  • cortical ribbons
  • PSWC
115
Q

which codon polymorphisms increase chance of prion infections

A

codon 129

116
Q

familial CJD defined by

A
  • CJD
  • CJD in family member
  • disease causing PRNP mutation
117
Q

brain stroke is a condition that occurs when

A

there is not enough blood flow to the brain to meet metabolic demand
* leads to limited oxygen supply and death of brain tissue

118
Q

_ strokes are more common

A

isochemic

119
Q

ischemic strokes are due to

A

blockage of blood vessel

120
Q

hemorrhagigc strokes are due to

A

bleeding around the brain

121
Q

most common symtoms of stroke

A

all are sudden
* numbness of face arm or leg
* confusion
* trouble seeing
* dizziness
* severe headache

122
Q

arteries bringing blood to the brain

A
  • internal carotid artery
  • vertebral artery
  • the circle of willis
123
Q

middle cerebral artery

A
  • covers 80% of lateral surface of the brain
  • common site of occlusion
124
Q

anterior cerbral artery

A
  • mostly supplies the midline of both cerebral hemispheres
125
Q

posterior cerebral artery

A
  • supplies the parietooccipital and temporal cortices
126
Q

advantage of the circle of willis

A
  • connects everything so if there is occulusion other branches can provide blood to the vital areas
127
Q

the major arteries giving blood to the brain make up the

A

circle of willis

128
Q

ischemic penumbra

A

outside part of affected region by stroke
* can recover after if treatment is fast enough
* will become core (dead) if not fast enough

129
Q

in stroke, tissue outcome depends on

A
  • severity of flow reduction
  • duration of flow reduction
130
Q

statistics of stroke

A
  • very common cause of death
  • aging is a risk factor
  • leading cause of disability
131
Q

CADASIL

A
  • inherited form of cerbrovascular disease
  • occurs when the thickening of blood vessel walls blocks the flow of blood to the brain
  • genetic risk factor for stroke
132
Q

CADASIL

A
  • inherited form of cerbrovascular disease
  • occurs when the thickening of blood vessel walls blocks the flow of blood to the brain
  • genetic risk factor for stroke
133
Q

imaging used to see stroke

A

FLAIR MRI

134
Q

CADASIL mutation causes

A
  • mutation in substrate for gamma secretase (NOTCH 3)
135
Q

ischemic cascade in the core

A
  1. ENergy failure (decrease in ATP)
  2. decrease in Na/K ATPase
  3. anoxic deplarization (constant APs)
  4. increased glutamate release
  5. excitotoxicity
136
Q

penumbra ischemic cascade

A

stress increases glutamate release
* leads to excitotoxicity, apoptosis and necroptosis

137
Q

temporal sequence of events in cerebral ischemia

A
  1. excitotocity within minutes, falls at hours
  2. release of GABA to inhibit glutamate during exocitocity
  3. depolarization constant whole time
  4. inflammation after hours
  5. necroptosis and apoptosis increase as time goes on
138
Q

mechanisms of ischemic cell death in the brain

A
  • activation of cytokines, proteases
  • cell swelling
  • excitoxicity
  • transmigration of immune cells
139
Q

stages of excitotoxicity

A
  • initiation: increase in glutamate
  • amplification release of Ca and Ca up in cell
  • expression: ROS, RNS, swelling, yeet cell
140
Q

proinflammatory cytokines

A
  • IL 1, 6, TNF
141
Q

cell death and immune response in isochemic

A
  • proinflammatory responses
  • proinflammatory cytokines
  • leukocyte infiltration
  • tissue damage
142
Q

resolution of inflammation and tissue repair

A
  • clearing dead cells with “eat me” and “find me” signals
  • releasing anti inflammatory cytokines (IL 10, TGF beta)
  • brain repair (MMPs)
143
Q

rt-PA (activase)

A
  • clot buster
  • drawback: need to administer within 3 hours and only worls for isochemic stroke
144
Q

current strategies of stroke treatment target

A
  • oxidative stress
  • excitotoxicity
  • apoptosis
  • inflammation
  • energy deficit
145
Q

_ plays a key role in ischemic mechanisms

A

inflammation

146
Q

cell death type in infarct core

A

necrosis

147
Q

two broad groups of cerebrovascular disease

A
  • ischemia
  • hemorrhage
148
Q

potential ways to harness the human microbiome

A
  1. stool from two groups then analysis
  2. put stool from patients in animal modes and behav anal
  3. transfer healthy stool to patients and behav analy
  4. control diet of patients
149
Q

98% of the gut biome

A
  • firmicutes
  • bacteroidetes
150
Q

estabilishment and maintainence of gut colony

A
  • high variability in infancy
  • higher diversity in species as we age
151
Q

estabilishment and maintainence of gut colony

A
  • high variability in infancy
  • higher diversity in species as we age
152
Q

the microbiota gut brain axis

A

bidirectional communication
* HPA axis
* bacteria release neurotransmitters and neuropeptides, microbial by products and metabolites, cytokines, bacterial debris

153
Q

the microbiota gut brain axis

A

bidirectional communication
* HPA axis
* bacteria release neurotransmitters and neuropeptides, microbial by products and metabolites, cytokines, bacterial debris

154
Q

microbiome and aging

A
  • aging affects microbiomes and their products which effects intestinal properties
  • which causes increased frailty, inflammaging, release of proinflammatory cytokines, increased blood pressure
155
Q

microbiome and aging

A
  • aging affects microbiomes and their products which effects intestinal properties
  • which causes increased frailty, inflammaging, release of proinflammatory cytokines, increased blood pressure
156
Q

centenarians have an

A

overall higher diversity in their microbiome, but not necessarily the same as the young microbiome

157
Q

centenarians have an

A

overall higher diversity in their microbiome, but not necessarily the same as the young microbiome

158
Q

centenarians have an

A

overall higher diversity in their microbiome, but not necessarily the same as the young microbiome

159
Q

centenarians have an

A

overall higher diversity in their microbiome, but not necessarily the same as the young microbiome

160
Q

centenarians have an

A

overall higher diversity in their microbiome, but not necessarily the same as the young microbiome

161
Q

germ free mice never

A

develop mature microglia

the microbiome affects microglial maturation and activation

162
Q

microbiota secrete

A

ROS scavengers
* short chain fatty acids
* ferulic acid

163
Q

microbial dysbiosis

A

leaky gut so increase in proinflammatory molecules which increases BBB ermeability which causes oxidative stress in CNS

164
Q

_ shows lewy body pathology first in PD

A

dorsal motor nucleus of CN10

165
Q

_ starts to show lewy body pathology in PD stage 3

A

substantia nigra

166
Q

dual hit staging hypothesis

A

PD pathology originates from insults in the peripheral organs where alpha syn is seeded before translocating to the brain

167
Q

patients with IBS show

A

an increased incidence of PD

evidence for the dual hit staging hypothesis

168
Q

evidence for dual hit staging hypothesis in animal models

A
  • gut microbes promote alpha syn mediated motor deficits and brain pathology
  • depletion of gut bacteria reduces microglia activation
  • human gut microbiota from PD patients enhanced motor dysfunction in mice
169
Q

limitations of microbiota research

A
  • defing normal and healthy gut microbiota
  • understand the effect of lifestyle
  • define directionality between cause and effect
  • understand the contribution of gene enviroment impacts
  • understand the effect of lifestyle
170
Q

gut microbiome

A

A collection of microorganisms, viruses, and fungi, their genes and genomes

171
Q

There has been evidence for a role for the microbiome in which of the following disorders?

A

Parkinson’s Disease
Alzheimer’s Disease
Multiple Sclerosis
Amyotrophic Lateral Sclerosis

172
Q

primary pathways by which the gut microbiome may modulate neurodegenerative diseases

A
  • The immune system
  • The vagus nerve
  • Microbial metabolites in circulation

NSCI 4501 (5 decks)

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