Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/44314
Full metadata record
DC FieldValueLanguage
dc.contributor.advisorBrône, Bert-
dc.date.accessioned2024-09-25T08:23:07Z-
dc.date.available2024-09-25T08:23:07Z-
dc.date.issued2024-
dc.date.submitted2024-09-24T09:57:11Z-
dc.identifier.urihttp://hdl.handle.net/1942/44314-
dc.description.abstractThis thesis focuses on two pivotal facets of the pathophysiology of schizophrenia. Firstly, it examines the impact of glial cell involvement on the disruption of neuronal circuits. Secondly, it elucidates the mechanisms underlying glial cell dysfunction through a comprehensive exploration of the etiology of schizophrenia. Employing a dual approach, it integrates a genetic mutation with microglial cells to uncover the cellular component of inflammation driving cognitive symptoms in schizophrenia. Simultaneously, it investigates how astrocytes serve as conduits for soluble inflammatory markers, studying their influence on the manifestation of positive symptoms in schizophrenia.-
dc.language.isoen-
dc.titleGlia-neuron interactions as pathophysiological mediators of schizophrenia-
dc.typeTheses and Dissertations-
local.bibliographicCitation.jcatT1-
local.type.refereedNon-Refereed-
local.type.specifiedPhd thesis-
local.provider.typePdf-
local.uhasselt.internationalno-
item.fullcitation (2024) Glia-neuron interactions as pathophysiological mediators of schizophrenia.-
item.accessRightsEmbargoed Access-
item.fulltextWith Fulltext-
item.embargoEndDate2029-09-27-
Appears in Collections:Research publications
Files in This Item:
File Description SizeFormat 
Dissertation_ChloëTrippaers.pdf
  Until 2029-09-27		Published version4.47 MBAdobe PDFView/Open    Request a copy
Show simple item record

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.