Deciphering the role of NF-κB and STAT-1/3 in the pathology of a murine model of Lewy Body Dementia
Publication Date
July 19, 2019
Creator
Abstract
This study was conducted to investigate and further understand the precise relationship between selected members of the transcription regulating families of both NF-kB and STAT in promoting neuroinflammation. This was attempted by measuring differences in the co-localisation of the selected proteins alongside the proliferative hypertrophy of astrocytes known as astrogliosis. Results were acquired using a previously generated ‘neuronal-specific Ubiquitin proteasome pathway (UPP) -dysfunctional mouse model of Lewy Body Dementia’. Findings show a significant increase in astrogliosis within the model. Furthermore it was observed that STAT-1 and STAT-3 have time-dependant differences in protein expression. However, definitive altered pathway regulation differences were not observed, thus a robust definition of this relationship could not be established.
NF-kB could not be consistently detected suggesting an absence or unimportance in the model. This absence also hints at a potential experimental flaw, due to the ubiquitous nature of NF-kB. Ultimately, the observations recorded in this study do not present a definitive means by which the UPP dysfunction dependent inflammation of the CNS is increased by virtue of NFkB nor STAT proteins.
Item Type
ethesis
Thesis Type
MRes
Supervisors
Subjects (LC)
Associated Schools / Departments
School of Life Sciences
eprints ID
56955
UoN Repository URI
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