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Title: The role of basal autophagy in oligodendrocyte development
Author: Yang, Cheng
ISNI:       0000 0004 8507 9482
Awarding Body: UCL (University College London)
Current Institution: University College London (University of London)
Date of Award: 2019
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Neurodegenerative diseases can be caused by abnormal protein accumulation, mitochondrial dysfunction and intracellular oxidative stress, all of which fall within the realm of autophagy, including autophagic clearance of protein aggregates and autophagic degradation of organelles (e.g. mitophagy). Although the exact mechanisms regulating autophagy in the central nervous system (CNS) remain unknown, it is likely that autophagy failure plays a critical role in the pathology of neurodegenerative disease. This study investigates the role of basal autophagy in oligodendrocyte (OL) development and OL function, focusing on autophagic activity in OL lineage cells and the effect of autophagy on OL production during OL development and in adulthood. It has been reported that myelinophagy, a recently discovered form of selective autophagy, is involved in the degradation of myelin and promotes myelin clearance in the peripheral nervous system (PNS). My current study also examines the role of autophagy in myelination, which has not yet been well investigated. We generate mice lacking autophagy related gene 5 (Atg5) specifically in OL lineage cells to study the role of autophagy in OL development and OL function. Employing immunostaining, electron microscopy and lipidomics analysis, we found that although the loss of autophagy does not have an evident effect on the proliferation and differentiation of OL precursors during OL development, it can cause abnormal aggregations of intracellular proteins in adult-born OLs with age, indicating that autophagy primarily affects adult-born OL function. In addition, a number of astrocytes become reactive in the cortex of these mice, which is the hallmark in response to the CNS pathologies, hinting at the importance of OL autophagy in maintaining brain homeostasis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available