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Genetic factors influencing oligodendrocyte demyelination

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TitleInfo
Title
Genetic factors influencing oligodendrocyte demyelination
Name (type = personal)
NamePart (type = family)
Yu
NamePart (type = given)
Qili
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Qili Yu
Role
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author
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NamePart (type = family)
Zhou
NamePart (type = given)
Renping
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Renping Zhou
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Advisory Committee
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chair
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Dreyfus
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Cheryl
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Cheryl Dreyfus
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Advisory Committee
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internal member
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Kusnecov
NamePart (type = given)
Alexander
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Alexander Kusnecov
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Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Pang
NamePart (type = given)
Zhiping
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Zhiping Pang
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Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Cai
NamePart (type = given)
Li
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Li Cai
Affiliation
Advisory Committee
Role
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outside member
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Rutgers University
Role
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degree grantor
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School of Graduate Studies
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school
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Text
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theses
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DateCreated (qualifier = exact)
2018
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2018-01
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2018
Place
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xx
Language
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eng
Abstract (type = abstract)
Oligodendrocytes are an important cell type in the central nervous system (CNS). Their most prominent function in the brain is to provide axonal processes of neurons with insulation by means of creating myelin sheath that wrap around axons (myelination), which serves to increase the nerve conduction velocity, as well as to provide trophic support. Due to their high metabolic demand, oligodendrocytes are particularly susceptible to demyelinating pathology, the most prominent ones being multiple sclerosis and various leukodystrophies. Thus understanding the genetic and molecular factors that contribute to oligodendrocyte demyelination is crucial to our understanding of the diseases and identification of therapeutic targets. In order to address this issue, we conducted two studies in an attempt to elucidate the factors that are involved in regulation of the demyelination process in the CNS. Our first approach involves challenging two different mouse strains (C57BL/6 and CD1), which have different genetic backgrounds, with the neurotoxin cuprizone to induce a multiple sclerosis (MS)-like demyelinating pathology in the corpus callosum. We show that cuprizone induced demyelination is highly strain-dependent, and thus is under significant influence of genetic background factors. Our second approach involves probing the developmental as well as the cuprizone induced demyelinating phenotype in mice devoid of a gene that is highly expressed within CNS myelin, namely, Ephrin-B3. Our results suggest that Ephrin-B3 knockout animals exhibit relatively normal myelin-related phenotype compared to age-matched control animals, indicating that the gene is not specifically involved in regulation of oligodendrocyte myelination/demyelination in the CNS. Along the way, we document in this dissertation another separate study that aims to probe the developmental function of a gene named Fbxl15, which is a mammalian homolog of the drosophila jetlag gene, by way of gene-specific knockout study. We report here that Fbxl15 loss of function does not explicitly impact the circadian regulation in mice, and nor does it affect behavioral parameters in mice such as learning and memory, anxiety and depressive behavior. Thus we speculate that the function of Fbxl15 is redundant throughout development and that other F-box proteins could compensate for the absence of Fbxl15.
Subject (authority = RUETD)
Topic
Neuroscience
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Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_8562
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xvi, 119 p. : ill.)
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Subject (authority = ETD-LCSH)
Topic
Multiple sclerosis
Note (type = statement of responsibility)
by Qili Yu
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3W09943
Genre (authority = ExL-Esploro)
ETD doctoral
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Rights

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The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Yu
GivenName
Qili
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2017-12-14 17:14:28
AssociatedEntity
Name
Qili Yu
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical

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2017-12-15T16:41:15
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2017-12-15T16:41:15
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