Date of Award
2015
Document Type
Dissertation/Thesis
Submission Date
October 2026
Thesis/Dissertation Advisor [Chair]
Kirchman, Paul
Abstract
Intellectual disability (ID) is a neurodevelopmental disorder characterized by significant limitations in both adaptive behavior and intellectual function that arises prior to reaching adulthood. Studies revealed a prevailing correlation between patients with ID and a sporadic SYNGAP-1 gene mutation. The SYNGAP-1 gene encodes for the protein SYNGAP that controls intracellular signaling and is directly linked with synaptic transmission. Mouse models were used to analyze the structure of somatosensory cortical neurons in different layers of the cortex during brain development. Neurons of SynGAP-1 mutant mice in layer V of the somatosensory cortex displayed a much more complex structure than the wildtype during development but no differences once they reached adulthood. Adversely, in layer II/III, the neurons of mutant mice were less complex during the developmental stages. This research suggests that a SynGAP-1 haploinsufficiency causes ID by disrupting the natural timing of neuronal growth and brain development.
Recommended Citation
Shotwell, Kaitlyn, "Cortical Development in an Intellectual Disability (ID) Mouse Model" (2015). Harriet L Wilkes Honors College Theses 2010 - 2019. 239.
https://digitalcommons.fau.edu/etd_honors_2/239
Extent
29 p.
Identifier
FA00003655
Comments
Includes bibliography.