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NSCI 4501 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

2 basic elements of the immune system

A
  1. White Blood Cells or leukocytes
  2. Soluble mediators
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2
Q

Types of leukocytes (name/list)

A
  • neutrophil
  • eosineophil
  • basophil
  • lymphocyte
  • monocyte
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3
Q

3 types of lymphocytes

A
  • B cells
  • T cells
  • Natural killer cells
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4
Q

B cell function

A
  • binds to antigen
  • multiplies and differentiate into plasma cells
  • plasma cells make antibody
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5
Q

Th1 T cells function

A

interacts with monocytes and helps them destroy introcellular pathogens

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6
Q

Th2 T cells function

A

interacts with B cells and helps them divide

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7
Q

Cytotoxic T cells function

A

destructs host cells that have become infected by viruses or other things

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8
Q

Regulatory T cells function

A
  • help control the development of immune responses
  • decrease reaction against self tissues
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9
Q

Natural Killer cells function

A
  • recognize surface changes on tumor & viral-infected cells
  • damage those cells
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10
Q

Monocytes function depends

A

on location

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11
Q

Monocytes _ antigens

A

internalize antigens

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12
Q

B cell _ antigens

A

bind to antigens

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13
Q

Monocytes are derived from

A

bone marrow stem cells

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14
Q

Monocytes/Macrophages destroy by

A

engulfing and internalizing agents and tissue debris

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15
Q

Monocytes release _

A

inflammatory mediators (like Cas 1)

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16
Q

Antibodies structure

A
  • 4 polypeptide chains
  • 2 identical light chains, 2 heavy chains
  • 3 domains
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17
Q

Circulating antibodies are

A

soluble glycoproteins that recognize and bind antigens specifically

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18
Q

5 classes of antibodies in mammals

A
  • IgG
  • IgM
  • IgA
  • IgD
  • IgE
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19
Q

Complement proteins are

A

a group of 20 soluble proteins who control inflammation

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20
Q

Alternative pathway

A

pathway in which a number of microorganisms
spontaneously activate the complement system

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21
Q

Classical pathway

A

complement system activation pathway that is activated by antibodies bound to the
pathogen surface

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22
Q

The classical pathway of activating the complement system depends on

A

antibodies

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23
Q

the complement pathway kills pathogens by

A

decreasing membrane integrity

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24
Q

Functions of complementary proteins

A
  1. Lead to efficient development of antibody responses.
  2. Kill microbial microorganisms.
  3. Attract phagocytes by chemotaxis, triggering and amplification of inflammatory reactions.
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25
Q

Cytokine is the general term for

A

a large group of secreted molecules involved in signaling between cells during immune response.

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26
Q

all cytokines are

A

proteins or glycoproteins

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27
Q

Name some of the cytokine groups

A
  • interferons (IFN)
  • interleukins (IL)
  • chemokines
  • colony-stimulating factors
  • tumor necrosis factors
  • transforming growth factors
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28
Q

type 1 IFN

interferons

A

IFN⍺
IFNβ

  • can be produced by any cell
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29
Q

type 2 IFN

A

IFN𝛾

  • stronger than type 1
  • must go through antigen presenting
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30
Q

IFN that starts with a virus

A

IFN⍺
IFNβ

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31
Q

IFN that starts with an antigen

A

IFN𝛾

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32
Q

Th0 makes _ with _

A

Th0 makes Th1 with IL12 and IFNy

  • makes Th2 with IL4
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33
Q

Th1 promotes B cell what stages with what

A

Th1 promotes B cell division with IL2 and differentiation with IFNy

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34
Q

Th2 promotes B cell which stages and with what

A

Th2 promotes division with IL4
and differentiation with IL 4,5,6,10,13

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35
Q

innate immune response definition

A
  • does not depend on immune recognition
  • unspecific
  • provides immediate defense
  • not long last immunity
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36
Q

innate immune response mechanisms/symptoms/characteristics

A
  • inflmmation
  • phagocytosis
  • clearance of debris & pathogens
  • remodeling and regneration of tissues
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37
Q

adaptive immune response definition

A
  • depends on immune recognition by lympocytes
  • uses specific entigens
  • pathogens that do not have patterns can still be recognized
  • allows vaccines
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38
Q

T cells only recognize antigen peptides bound to

A

HLA encoded molecules

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39
Q

4 types of T cell activation

A
  • adhesion
  • Ag specific
  • costimulation
  • cytokine signaling
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40
Q

memory cells are

A

B cells that do not differentiate into plasma cells
* in an inactive state in host for a while

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41
Q

vaccines use

A

a modified pathogen that has antigens but cant do damage

called toxoids

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42
Q

purpose of inflammation

A
  • eliminate initial cause of injury
  • clear out necrotic cells
  • initiate tissure repair
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43
Q

acute inflammation is initiated by

A

resident immune cells like macrophages

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44
Q

macrophages contain _ so initiate inflammation

A

toll like receptors which recognize pathogen and damage associated molecular patters (PAMP and DAMP)

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45
Q

cytokine and chemokine lead to

A

leukocyte margination and enthelial adhesion

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46
Q

chemokines function as _

A

chemotactic mediators and attract leukocyte to infammatory sites

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47
Q

in response to inflammation, leukocytes

A

destroy pathogens and remove damaged tissues

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48
Q

lymhocytes are activated by

A

antigen presenting cells

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49
Q

chronic inflammation definition

A
  • persistent inflammation due to non degradable pathogens, viral infections or autoimmune reactions
  • adaptive immunity plays a major role
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50
Q

chronic inflammatory sites are characterised by

A

simultaneous destruction and repair of the tissue

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51
Q

Glia in the CNS

A
  • oligdendrocytes
  • microglia
  • astrocytes
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52
Q

Glia in the PNS

A

schwann cells

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53
Q

microglia are major in

A

brain and spinal cord

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54
Q

_ are derived from bone marrow stem cells

A

microglia

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55
Q

microglia are derived from

A

bone marrow stem cells

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56
Q

microglia can

A
  • act as first form on innate immune response in CNS
  • function as a APC and activate adaptive imm res in CNS
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57
Q

functions of microglia

A
  • Scavenging, survey CNS on a regular basis.
  • Phagocytosis, engulf tissue debris and invading pathogen.
  • Cytotoxicity, release cytotoxic substances to damage cells.
  • Inducing inflammation, release inflammatory mediators.
  • Antigen presentation, activate adaptive immune response.
  • Synaptic stripping, remove dysfunctional synapses.
  • Promoting repair, release growth factors.
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58
Q

M1 microglia are activated by

A

LPS and IFNy

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59
Q

M1 microglia promote

A
  • ROS
  • inflammatory cytokines
  • TNFa, IL1 & IL6
  • iNOS
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60
Q

M2 microglia activation

A
  • alternative activation: IL4 & IL13
  • aquired deactivation: IL10 & TGF beta
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61
Q

M2 microglia does what

A
  • engulfs pathogen
  • inhibits the things M1 does
  • activate neurotrophic growth factors
  • activate ECM reconstruction & tissue repair
  • activate Arg1
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62
Q

Arg 1 inhibits

A

iNos

and visa versa

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63
Q

functions of astrocytes

A

Structural: Maintain the physical structuring of the brain.
* Glycogen fuel reserve buffer: contain glycogen and are capable of
glycogenesis, can fuel neurons with glucose.
* Metabolic support: provide neurons with nutrients such as lactate
* Blood–brain barrier.
* Transmitter uptake and release: glutamate, GABA, etc.
* Regulation of ion concentration in the extracellular space: potassium
* Modulation of synaptic transmission.
* Nervous system repair.
* Long-term potentiation, modulate synaptic plasticity.

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64
Q

Blood brain barrier structure

A

endothelium then pericyte on tope then astrocyte on top

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65
Q

Gliosis

A
  • nonspecific reactive change in response to damage to the CNS
  • involves the proliferation and/or hypertrophy
  • lead to the formation of a glial scar
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66
Q

astrocyte end feet purpose

A
  • Providing biochemical support to endothelium.
  • Act as a physical barrier against unwanted cells or molecules
    attempting to enter the CNS.
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67
Q

functions of BBB

A
  • Restricts ionic and fluid movements between the blood and the brain, allowing specific ion transporters and channels to
    regulate ionic traffic, to produce a brain interstitial fluid that
    provides an optimal medium for neuronal function.
  • Act as a physical barrier against pathogen to enter the CNS.
  • Restricts entry of cytokines and chemokines into the CNS.
  • Restricts entry of leukocytes into the CNS.
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68
Q

_ are too large to cross the BBB.

A

Antibodies

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69
Q

why is the CNS have bad immunity

A
  • BBB too good
  • low levels of leukocyte into CNS
  • low level of MHC moleculed (not enough antigen presentation)
  • no lymphatic drainage system
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70
Q

MRI measures

A

water in the tissue

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71
Q

MRI how it works

A
  • magnetic properties of the protons in the water
  • put water in magnetic field, they line up with the field
  • then you send radio frequency to exicte and watch how they move back to alignment
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72
Q

in MRI, higher magnetic fields…

A

give higher resolution

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73
Q

TH1 weighted MRI images mechanism

A

uses the interaction of nuclei with its surroundings (lattice)
* T1 is time constant

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74
Q

T2 MRI images mechanism

A

uses spin spin interactions between nuclei

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75
Q

T1 vs T2 weighted: CSF

A
  • T1: Dark
  • T2: Bright
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76
Q

T1 vs T2 weighted: White Matter

A
  • T1: light
  • T2: dark grey
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77
Q

T1 vs T2 weighted: inflammation

A
  • T1: dark
  • T2: bright
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78
Q

_ is good for watching real time effects in brain

A

fMRI

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79
Q

fMRI mechanism

A

BOLD effect:
* when brain part is activated, blood flow increases in that region
* decrease in deoxyhemoglobin
* increase in fMRI signal

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80
Q

_ is good for mapping connections in the brain and seeing axonal damage

A

diffusion MRI

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81
Q

diffusion MRI mechanism

A
  • neasures anisotropic water diffusion in the brain
  • water diffuses along axons
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82
Q

low anisotrophy =

A

slower diffusion

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83
Q

diffusion in isotropic vs anisotropic samples

A
  • isotropic diffusion is all directions
  • anisotropic diffusion down axons
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84
Q

magnetic resonance spectroscopy (MRS) mechanism

A
  • supress H2O signal
  • get NM signal from other things
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85
Q

PET requires a _

A

substrate labeled with positron emitting tracer

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86
Q

PET mechanism

A
  • tracer emits positron
  • positron collides with electron
  • produces 2 photons traveling in oposite directions
  • 360 detectors used to map the photons and creat 3D images
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87
Q

the _ is very important in PET tracers

A

half life

tells you how long between admin tracer and doing scan

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88
Q

way to asses atrophy

A

structural MRI, T1 weighted

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89
Q

thing for assessing neuronal loss

A

MRI: volumetry, cortical thickness or MRS w/NAA, Glu

90
Q

microstructural changes can be assesed by

A

non-conventional MRI

91
Q

way to asses neuronal viability

A

MRS

looking at ratio of neurotransmitters (ex)

92
Q

assessing synaptic dysfunction

espicially in parkinson’s

A
  • dopamine PET or
  • MRS (MRI) with Glu, Gln or GABA
93
Q

_ can be used to asses _ in PD

A

PET to asses dopamine function in striatum

94
Q

demylination can be imaged by

A

MT MRI

95
Q

MRI can noninvasively image…

A
  • anatomy
  • blood flow
  • neuronal activation
  • connectivity
  • axonal damage
  • demylination
  • chemical levels
96
Q

PET can image…

A
  • metabolism
  • ligand binding
97
Q

Way to assess oxidative stress

A

MRS with glutathione (GSH) and ascorbate (Asc)

98
Q

_ are the most abundant antioxidants in CNS

A

GSH and Asc

99
Q

way to assess impaired energetics

A
  • FDG-PET
  • 31P-MRS (phosphate tracking)
  • 13C-MRS (Glu/GLn cycle rate)
100
Q

how does FDG PET assess what it does?

A

PDG PET traces wither glucose is phosphorylated or not which shows whether energetics (glucose uptake) are impaired

101
Q

Low FDG uptake is an indicator of _ in what diseases?

A
  • low FDG uptake = impaired energetics
  • could mean atrophy
  • AD, Dementia with Lewy Bodies (DLB), Frontotemporal Dementia (FTD)
102
Q

FDG-PET is useful in HD for…

A

detection of hypometabolism before symptoms

103
Q

what is a good technique for telling what ype of dementia patients have

A

FDG-PET

104
Q

phosphoros nuclei can help differentiate as specific as

A

different phaspates in ATP, so can see when ATP -> ADP or visa versa

105
Q

31P-MRS is useful for _ in PD

A

looking at levels of ADP and ATP (to assess energetics) in PD patients

106
Q

13C-MRS mechanism and what it shows

A
  • label C 13 on glucose to trace
  • can measure glutamate and glutamine levels with MR
  • can show if glucose metabolism is impaired (in AD)
107
Q

13C-MRS can show _ in AD

A

13C-MRS can show energy deficiets and slower metabolism as a cause of demetia that is in AD

108
Q

AD pathology

A
  • amyloid plaques
  • neurofibrillary tangles (NFTs)
  • diagnosis based on ^ and age and medical history

NFTs from tau protein aggregates

109
Q

_ can be used to asses toxic protein accumulation

A

11C-Pittsburgh compound B tracing with PET

PiB

110
Q

11C-Pittsburgh compound B binds to

A

Aβ plaques (extracellularly)

markers of AD

111
Q

order of biomarkers in AD progression

A
  1. Aβ amyloid plaques (PiB)
  2. tau NFTs (in CSF)
  3. Dementia (MRI & FDG-PET)
  4. Cognitive impairment
112
Q

tau deposition can be imaged by

A

using PET to see the density of NFT

113
Q

way of assessing gliosis

A
  • MRS with myo-inositol & Glutamine
  • PET w/ MAO-B
114
Q

way to assess reactive astrocytosis

A
  • MAO-B by PET
  • MRS MRI with myo-inositol and Gln
115
Q

MOA-B is localized in..

A

astrocytes

but people have them in other places too, increased MOA-B = AD

116
Q

MOA-B is localized in..

A

astrocytes

but people have them in other places too, increased MOA-B = AD

117
Q

way to assess neuroinflammation

A
  • TSPO by PET (acute inflammation)
  • Dynamic contrast enhanced (DCE) MRI (show BBB breakdown)
118
Q

TSPO is localized in _ and functions

A

glial cells and is upregulated with microglial activation

119
Q

DCE MRI requires…

A

a gadolinium based contrast agent

120
Q

DCE MRI shows _ by _

A
  • use agent to see leakage of in BBB
  • enhanced signal - BBB broken down
121
Q

MRI or PET uses ionizing radiation

A

PET

122
Q

MRI mostly does not use a tracer except

A
  • DCE MRI (contrast agent)
  • 13C-MRS (metabolism)
123
Q

PET does or does not use a tracer

A

always uses a tracer

non endogenous signal

124
Q

does MRI or PET have specific, molecular binding

A
  • MRI: depends
  • PET always does
125
Q

is MRI or PET more sensitive and why

A

PET is more senitive due to the tracer concentration (can be little)

126
Q

does MRI or PET have better resolution

A

MRI

127
Q

is MRI or PET cheaper/more available and why

A

MRI because tracers are expensive

128
Q

demylination can be imaged by

A

MT MRI

129
Q

anticipation is

A

a clinical phenomenon describing progressively earlier onsent of the disease in successive gnerations

130
Q

symptoms of fragile X syndrome

A
  • abnormal facial feature
  • cognitive defiecits
  • disability
  • shyness, poor eye contact
131
Q

TRE in gene FMR1 causes gain or loss of the FRMP1 protein

A

causes loss of FRMP1 protein function

this causes Fragile X syndrom

132
Q

TRE in gene DMPK causes gain or loss of DMPK RNA function

A

causes gain of DMPK function

this causes Muscular Dystrophy 1

133
Q

_ in the DMPK gene is responsible for what disease

A

TNE in DMPK causes Muscular Dystrophy 1

134
Q

TRE in gene FMR1 causes

A

fragile X syndrome

135
Q

HD is caused by

A

an TNE in the HTT gene

136
Q

Ataxia is a disease that effects

A

the cerebellum

137
Q

HD effect

brain part

A

basal ganglia

138
Q

In HD, up to 95% of _ are lost

A

GABAergic medium spiny projection neurons

139
Q

factors influencing TNR diseases’ phenotypes

A
  1. germline instability (not stablely transmitted mutation)
  2. larger expansion = earlier onset
140
Q

anticipation

A

progressively earlier onset of diease in sucessive generations

happens in TNR diseases

141
Q

TNR in promoter

(effect and disease example)

A
  • transcriptional silencing
  • loss of function
  • fragile X syndrome
142
Q

TNR in intron

(effect and disease example)

A
  • impaired transcription
  • ** friendreich ataxia**
143
Q

TNR in coding region

(effect and disease example)

A
  • expanded PolyQ
  • gain of function
  • huntington disease
  • SCA 1, 2, 3
144
Q

TNR expansion at end of exon

(effect and disease example)

A
  • new RNA properties
  • gain of function
  • mytonic dystrophy
145
Q

fragile X syndrome is _ function due to TNR in _ gene

A
  • loss of protein function
  • FMR1 gene
146
Q

Fragile X syndrome features/symptoms

A
  • abnormal facial structure
  • anxiety
  • hypersensitivity
  • disability
  • autistic features: shyness, poor eye contact
147
Q

Fragile X syndrome genetic pattern

A
  • X linked dominant
  • less penetrance in females
148
Q

pathological hallmark of FX Syndrome

A
  • in cortex abnormal spines
  • elongated shafts and small heads
  • immauture spines
149
Q

FXS molecular mechanism

A
  • methylation and transcriptional repression of FMR protein
  • FMR protein blocks mRNA in binds to, decreasing signaling and endocytosis

in FXS
* FMR protein loss of function = ↑ signalling through mGlu (LTD) = ↑ mRNA = ↑ endocytosis of AMPA-R = immature spines

150
Q

lowering _ expression for FXS helped symptoms

A

lower mGlur expression with knock out mice

151
Q

treatment of FXS

A

mGluR antagonists

152
Q

Mytontonic Dystrophy Type 1 (DM1) clinical signs

A
  • Myotonia (impairement of relaxing muscles)
  • Muscular dystrophy
  • cardiorespitory problems
  • cataract
  • cognitive problems
153
Q

DM1 inheritance pattern

A

autosomal dominant

154
Q

DM1 is caused by TNR in and is a _ function mutation

A
  • DMPK gene
  • RNA mediated gain of toxic function
155
Q

MD1 mechanism

A
  • repeats in DMPK cause sticking of RNA spilicing factors (MBNL) to it
  • less MBNL = no splicing of certain genes
  • unstable proteins are expressed, toxic gain of function
  • loss of CIC-1 channel
156
Q

how does MD1 mechanism lead to mytonia

A

DM1 TNR
= ↓ MBNL splicing factor
= ↑ function of toxic gene
= ↓ CLC channels
= ↓ Cl permebaility
= ↑ excitability of muscle cells (no repolarization)

157
Q

DM1 therapeutic approaches

A
  • inhibition of RNA polymerase
  • other molecules that bind the repeats
  • ASO to post transcriptionally silence
158
Q

ataxia

A

loss of full control of bodily movements

159
Q

adult onset SCA1 clinical signs

A
  • ataxia
  • dysphagia (no swallow)
  • dysarthia (speech)
  • cognitive changes
160
Q

SCA1 pathology

A
  • atrophy of cerebellum (ataxia) and brain stem
  • loss of Purkinje neurons
161
Q

SCA1 inheritience

A

autosomal dominant

162
Q

Sca1 TNR is _ gene and causes _ function mutation

A

TNR in Sca1 causes gain of function in ATXN1 protein

163
Q

Decreasing ATXN1 during _ stage is beneficial

A

early and middle stages of Sca1

164
Q

decreasing ATXN1 in _ stages does not help _

A

decreasing in late stages does not help motor deficits in Sca1

165
Q

Sca1 therapies should be

what time

A

before onset of symptoms

166
Q

SCA1 mechanism

A
  • TNR = ↑ ATXN1
  • ATXN1 go in nucleus
  • ATXN1 regulates transcription and RNA splicing
167
Q

SCA1 therapeutic approaches

A
  • inhibit ATXN1 through phsphorylation
  • ASO to cut out TNR
168
Q

how does ASO work

A

ASO makes dsRNA to cut out a specific TNR extra parts

169
Q

HD is cause by _

A

caused by TNR in exon 1 of HTT gene which makes polyQ expansion in huntington protein

170
Q

HD inheritence

A

autosomal dominant

171
Q

HD genetics phenotypical differences

A
  • more repeats = ↓ age of onset
  • risk factors affect age of onset
172
Q

3 stages of HD

A
  1. presymptomatic
  2. predromal
  3. manifest
173
Q

Presymtomatic and prodomal stages of HD characterized by

A
  • subtle effects
  • cognitive
  • motor alternation
  • weight loss
174
Q

Manifest stage of HD characterized by

A
  • Motor symptoms: chorea, fine moter bad, slurring, akinesia later
  • cognitive symptoms
  • mood symptoms

chorea = involuntary movement, jerking

175
Q

Neuropathological hallmakrs of HD

A
  • volume & cell loss in striatum
  • dysfunction and death of MSN
  • presence of huntington protein aggregates
176
Q

CNS motory systems mechanism in HD

A
  • loss of indirect pathway MSN = loss of D2 receptors
  • D2 receptors inhibit GPe, so GPe uninhibited
  • STN activates Gpi, so GPi inhibited
  • GPi inhibits thalamus so disinhibition of thalamus s0 increase in motor cortex`

D2 ↓ = ↑ GPe = ↓ STN = ↓ GPi = ↑ thalamus = ↑ motor cortex

177
Q

loss of HTT gene causes

A

embryonic death

178
Q

mechanism of transcriptional problems in HD

A

TNR in Htt gene = polyQ expansion = Htt cannot associate with REST = no BDNF transcription

REST is repressor elemement
BDNF is a neurotrophic factor

179
Q

dysregulation of heat shock response in HD

A

mutant Htt = ↑ CK2⍺ = ↓ HSF1 = ↓ proteasomal degredation = ↑ protein misfolding = ↑ huntington aggregates

180
Q

HD palliative care techniques

A
  • tetrabenazine to treat chorea
  • things for cognitive
  • speech/physical therapy
181
Q

possible cures in animal models of HD

A
  • neuronal stem cell transplanation
  • Cas9 editing of gene
  • ASO gene silencing
182
Q

MS symptoms clinical

A

very wide variety

183
Q

clinical subtypes of MS

list off

A
  1. Relapsing Remitting MS (RR MS)
  2. Secondary progressive MS
  3. primary progressive MS
  4. progressive relapsing MS
184
Q

relapsing remitting MS

A
  • most common
  • no progressive decline
  • random episodes of severeness then nothing
185
Q

secondary progressive MS

A
  • bad episodes that are random with nothing in between
  • constant episode with variable severity
  • severity never to nothing but still declines and inclines constantly
186
Q

primary progressive MS

A

starts and gets worse without ever declining

187
Q

progressive relapsing MS

A
  • relapses worse over time
  • constant symtoms, no return to normal
  • small declines after relapse episode
188
Q

MS plaques pathology hallmarks

the cracks

A
  • inflammation
  • demyelination
  • oligodendrocyte death
  • axon degeneration
189
Q

symptoms in MS are variable because

A

pathology is localized by where in brain

190
Q

MS general pathology

A
  • demyelination
  • neurodegeneration
  • volume loss
  • cell death
191
Q

_ occurs early in MS

A

neurodegeneration

192
Q

causes of MS

list

A
  • genetics
  • enviromental factors
  • infectious factors
  • sex hormones
193
Q

genes involved in MS

A
  • HLA antigen presentation
  • T cell receptor antigen presentation
  • receptor for IL1, 2, 17
  • TNF⍺, β inflammation
194
Q

enviromental factors for MS

A
  • sunlight help increase good T cell activity
  • make vitamin D to inhibit autoimmune response (allergies)
195
Q

infectious factors for MS

A
  • epstein-barr virus
  • Human herpes simplex virus 6
196
Q

immune pathogenesis of MS

A
  • T cell mediated autoimmune demylination
  • myeline reactive T cells should only be in PNS, MS patients have in CNS also
197
Q

hypotheses of MS pathogenesis

A
  1. molecular mimicry
  2. by stander activation of APC which activate reactive T cells
  3. BBB breakdown
  4. oligodendrocyte death
198
Q

_ is decreased in the progressive stage of MS

A

inflammation

199
Q

progressive MS results from

A

neurodegeneration

200
Q

neurodegeneration in MS happens because

A

oligodendrocytes lost so demylination and MS has no remyelination so neuron is lost gradually

201
Q

MS can be diagnosed with _ to view _

A
  • MRI to see inflmmaion
  • CSF tests to see level of T/B cells
  • EP tests to see demylination
202
Q

short term treatments for acute relapse in MS

A

IV of glucocorticoids to inhibit inflammation by
* inhibition of antigen presentation
* reduction of edema
* decrease of proinflammatory cytokines
* inhibition of lymphocytes

203
Q

long term treatments of MS

A
  • IFN-β: inhibit T cell activation
  • Tysabri: block entry of lymphocytes in CNS
204
Q

treatmentss that _ are not available in MS

A

treatments that delay disability progression

205
Q

list animal models of MS

A
  • EAE
  • ciral models
  • neurotoxin models
206
Q

Q2. Antibodies are produced by

A

Plasma cells

207
Q

What type of cells initiates acute inflammation?

A

REsident monocytes (Macrophages)

208
Q

What form of energy is important for MRI?

A

Radiowaves

209
Q

The hallmark MR imaging biomarker for Alzheimer’s Disease is

A

hippocampal atrophy

210
Q

The most widely used approach to assess presynaptic dopamine function

A

imagining membrane dopamine transporters

211
Q

abnormal shape of the substantia nigra can be seen in _ with _

A

seen in PD with an MRI

212
Q

SCA1 is characterized by _ in _

A

severe loss of Purkinje neurons in the cerebellar cortex

213
Q

functional imaging can be used in HD to…

A
  • identify molecular biomarkers
  • assess brain atrophy
  • measure striatum volume
214
Q

Most common form of MS is

A

relapsing remitting MS

215
Q

treatments of MS aim to:

A
  • supress inflammation
  • protect oligodendrocytes and myeline
  • protect neurons and axons
216
Q

ATXN1[82Q]A776 mice

cannot be phosphorylated

A

no disease

217
Q

Gliotic activity can be imaged by

A
  • PET with TSPO
  • mI MRS MRI
  • PET with MAO-B
218
Q

mechanisms for remyleination failier in MS

A
  • chronic inflammation kills oligodendrocytes
  • microenviroment doesn’t allow O precursor cells to differentiate
  • OPC depletion
  • aging reducing OPC ability to remylinate
219
Q

animal Models of progressive MS

A
  1. EAE
  2. TMEV
  3. Caprizon
220
Q

immune players in MS

A
  • Th1, Th17
  • B cells
  • microglia
  • macrophages

NSCI 4501 (5 decks)

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