Year: 2015
Type: dissertation
Abstract: Fragile X syndrome (FXS) is the most common inherited form of mental impairment and the leading genetic cause of autism. Our laboratory has previously reported that myelination is delayed in the cerebellum of a mouse model of FXS. In my study, I assessed the spatial and temporal aspects of this myelination defect and found that the defect occurs throughout the brain in the early developing fragile X mouse. Additionally, I also examined the levels of epidermal growth factor receptor (EGFR) and two of its ligands but found little to no deficiencies in the fragile X brain. However, epidermal growth factor (EGF) levels in the plasma and thyroid of adult fragile X mouse were found to be significantly reduced. Lastly, the fragile X mice were treated with intranasal heparin binding EGF-like growth factor (HB-EGF) in an attempt to rescue the myelination defect but the treatment did not promote early postnatal myelination.
Source: TSpace (University of Toronto)
Author: David Lai Jiang
Language: English
Subfield: Genetics
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2611043128