• Deutsch
    • English
  • English 
    • Deutsch
    • English
  • Login
Item View 
  •   Home
  • Medizin
  • Human- und Zahnmedizin
  • Item View
  •   Home
  • Medizin
  • Human- und Zahnmedizin
  • Item View
JavaScript is disabled for your browser. Some features of this site may not work without it.

Die Rolle der Rezeptor-Protein-Tyrosin-Phosphatase Typ ζ bei der De- und Remyelinisierung

The role of the receptor protein tyrosine phosphatase type ζ (RPTPζ) for de- and remyelination

by Gero Lockstaedt
Doctoral thesis
Date of Examination:2013-10-28
Date of issue:2013-10-11
Advisor:Prof. Dr. Christine Stadelmann-Nessler
Referee:Prof. Dr. Christine Stadelmann-Nessler
Referee:Prof. Dr. Michael Werner Sereda
Referee:Prof. Dr. Rainer Mausberg
crossref-logoPersistent Address: http://dx.doi.org/10.53846/goediss-4071

 

 

Files in this item

Name:eDISS (Gero Lockstaedt).pdf
Size:1.82Mb
Format:PDF
ViewOpen

The following license files are associated with this item:


Abstract

English

Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by disruption of the blood-brain barrier, inflammation, demyelination, loss of oligodendrocytes, axonal damage and reactive gliosis. The extent of remyelination is highly variable between patients. The receptor protein tyrosine phosphatase type ζ (RPTPζ) is primarily expressed by oligodendrocytes, astrocytes and neurons in the CNS. Previous work has shown that RPTPζ seems to be important for myelin formation and remyelination in the context of recovery from experimental demyelinating diseases. This work examines the effects of RPTPζ deficiency in the cuprizone mouse model of toxic demyelination focusing on the extent of de- and remyelination, the loss of mature oligodendrocytes, the recruitment/differentiation of oligodendrocyte precursor cells, axonal damage and infiltration of CD3+-T-cells and activated microglia into the mouse corpus callosum. For this purpose demyelination was induced in wildtype and RPTPζ-deficient mice. We did not observe significant differences regarding the extent of de- and remyelination or the cellular processes listed above. In summary, the lack of RPTPζ does not influence the extent of de- and remyelination, the loss of mature oligodendrocytes, recruitment/differentiation of oligodendrocyte precursor cells, axonal damage or infiltration of CD3+-T-cells and activated microglia in the cuprizone model.
Keywords: RPTPζ; Multiple Sclerosis; Remyelination
 

Statistik

Publish here

Browse

All of eDissFaculties & ProgramsIssue DateAuthorAdvisor & RefereeAdvisorRefereeTitlesTypeThis FacultyIssue DateAuthorAdvisor & RefereeAdvisorRefereeTitlesType

Help & Info

Publishing on eDissPDF GuideTerms of ContractFAQ

Contact Us | Impressum | Cookie Consents | Data Protection Information
eDiss Office - SUB Göttingen (Central Library)
Platz der Göttinger Sieben 1
Mo - Fr 10:00 – 12:00 h


Tel.: +49 (0)551 39-27809 (general inquiries)
Tel.: +49 (0)551 39-28655 (open access/parallel publications)
ediss_AT_sub.uni-goettingen.de
[Please replace "_AT_" with the "@" sign when using our email adresses.]
Göttingen State and University Library | Göttingen University
Medicine Library (Doctoral candidates of medicine only)
Robert-Koch-Str. 40
Mon – Fri 8:00 – 24:00 h
Sat - Sun 8:00 – 22:00 h
Holidays 10:00 – 20:00 h
Tel.: +49 551 39-8395 (general inquiries)
Tel.: +49 (0)551 39-28655 (open access/parallel publications)
bbmed_AT_sub.uni-goettingen.de
[Please replace "_AT_" with the "@" sign when using our email adresses.]