Advisor(s)
Nina Kraguljac
Committee Member(s)
Christianne Strang
Gerhard Hellemann
Jarred Younger
Junghee Lee
School
College of Arts and Sciences
Document Type
Dissertation
Department (new version)
Psychology
Date of Award
9-11-2025
Abstract
It is well established that myelin in the central nervous system is an axonal insulator which speeds the conduction velocity of action potentials. However, its role in the cortex has also been shown to support metabolic demands and aid in cortical plasticity. Myelin develops throughout childhood and adolescence from sensorimotor areas to association areas and peaks during adolescence. Importantly, this is the same time that psychosis-spectrum disorders (PSDs) begin to present clinically; thus, given the critical role of myelination in shaping the mature cortex, disruptions in this process – particularly during adolescence – are thought to partially explain the onset of PSDs. Previous in vivo myelin mapping studies in PSDs have been inconclusive in describing myelin abnormalities due to inconsistencies in sample size, medication status, and differing methodology. The studies in this dissertation aim to clarify these findings by applying the T1w/T2w ratio to a group of antipsychotic medication-naïve, first-episode psychosis patients (FEP) and a group of people with chronic PSDs to elucidate changes at two stages of the illness. The first study used the T1w/T2w ratio to examine apparent myelin content across the whole cortex in the FEP group. The second study used the same method, accounting for the transmit bias field, a radiofrequency artifact, to examine cortical layers in FEP and chronic patients. We found that FEP display increased T1w/T2w ratio values primarily in association areas. We then found that FEP and chronic psychosis patients display increased T1w/T2w ratio values across three cortical layers, and that this finding was consistent across sensorimotor and association areas. Our findings suggest that: 1) myelin abnormalities, as measured by T1w/T2w ratio, are present at the early stages of the illness; 2) increased apparent myelin in association areas in FEP is consistent with the idea of adolescence as a critical period of development of PSDs; 3) increased myelin, specifically on parvalbumin-containing interneurons (PV+ INs), may lead to an imbalance of the excitatory and inhibitory signaling in the cortex, and; 4) increased myelin across all cortical layers highlights the potential involvement of pyramidal cells instead of, or in addition to, PV+ INs in the excitatory/inhibitory imbalance in PSDs. Taken together, the studies presented here provide insight into a potential early biomarker of PSDs. The results may inform treatment of PSDs by providing a specific mechanism, time-frame, and location for drug development.
ProQuest ID
Recommended Citation
King, Victoria Lynn, "Myelin Mapping In Psychosis" (2025). All ETDs from UAB. 7352.
https://digitalcommons.library.uab.edu/etd-collection/7352
