Degree Date

9-2023

Document Type

Dissertation - Public Access

Degree Name

Psy.D. Doctor of Clinical Psychology

Academic Discipline

Clinical Psychology - Florida School of Professional Psychology

First Advisor

Elizabeth Lane, Ph.D.

Second Advisor

Kathie Bates, Ph.D.

Abstract

Individuals diagnosed with posttraumatic stress disorder (PTSD) have demonstrated extinction-resistant symptoms and long-lasting impacts on the brain’s functional activity (Krystal et al., 2017; Stark et al., 2015). PTSD illustrates a strong relationship with cognitive functioning, and research has found lower parietal and hippocampal volume and deterioration in brain function and structure, resulting in executive dysfunction, attentional deficits, mood dysregulation, and memory difficulties (Krystal et al., 2017; Stark et al., 2015; Weiner et al. 2017). Sleep has been investigated to better understand its contribution to AD pathologies as well as its impact on PTSD treatment and prognosis. Although sleep’s functions are not widely understood, past studies have found that sleep aids in clearing waste, reconsolidating memories, and promoting neuronal connection (National Institute of Neurological Disorders and Stroke, 2006; Pace-Schott et al., 2015). Preliminary research by Weiner et al. (2017) has demonstrated worse global cognitive functioning, lower superior parietal volume, and lower amyloid positivity in people with PTSD, although preliminary results have not indicated PTSD as an increased risk factor for AD (Weiner et al., 2017). Therefore, further assessment of the differences between CSF amyloid, CSF ptau, and PTSD symptoms, specifically sleep, may expand current research on AD risk factors and biomarkers. A total of 179 participants were included in this study and were split into two groups: a PTSD group (n = 96) and a control group (n = 83). A MANCOVA analysis was conducted to assess if one or more mean differences between sleep quality index scores and AD pathology (i.e., CSF tau, CSF p-tau, CSF amyloid beta, CSF amyloid beta 40, and CSF amyloid beta 42/40 ratio) as well as in neuropsychological assessment results were present in a PTSD group compared to the control group (i.e., no PTSD or TBI group) among Vietnam veterans. A statistically significant MANCOVA effect was obtained, Pillai’s Trace = 0.28, ii F(6,61) = 3.89, p < 0.002, when assessing differences between sleep quality and AD pathology. However, a statistically significant MANCOVA effect was not obtained, Pillai’s Trace = 0.16, F(11,38) = 0.68, p = 0.75, when assessing differences on neuropsychological assessments. Findings from this study suggest that sleep disturbance is prominent in individuals with PTSD and could be a significant contributor to AD pathologies. However, no difference was found between groups on neuropsychological assessments, illustrating that individuals with PTSD do not differ from those without PTSD in areas assessed by these measures.

Comments

Acknowledgments Special thanks and appreciation are given to the Department of Defense Alzheimer’s Disease Neuroimaging Initiative (DOD ADNI) for allowing me access and utilization of their collected data on the Vietnam Veteran population, which was the basis for my research. My own study would not have been possible without their efforts to understand the connections between Traumatic Brain Injury (TBI), posttraumatic stress disorder (PTSD), and the signs and symptoms of Alzheimer’s disease among Vietnam Veterans. Their established data set enabled my dissertation to be completed, for which I am forever grateful.

It is also noted that data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech, BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Incs.; Cogstate; eisai Inc.’ Elan Pharmaceuticals, Inc.; Eli Lily and Company; Eurolmmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosit; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC,; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the iv Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.

Additionally, I am appreciative to each of the members of my Dissertation Committee, Drs. Elizabeth Lane and Kathie Bates, for their extensive personal and professional guidance, as well as the knowledge they have taught me about scientific research. I would be remiss in not mentioning that my research endeavors would also not have been possible without Dr. Elizabeth Lane’s research with the ADNI study that allowed me to have access to the DOD ADNI data set as well

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