Degree Date

6-2020

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, PhD

Second Advisor

Eric Rosen, PhD

Abstract

Mild cognitive impairment (MCI) is often a prodromal stage for Alzheimer’s disease (AD) development, with those diagnosed with MCI at increased risk for developing AD. The present study aimed to provide data to support a prodromal stage of MCI via analysis utilizing the neuropsychological domain of memory, subjective memory impairment (SMI), and the PET tau biomarker, AV-1451. It was hypothesized that individuals with SMI would differ significantly from participants without SMI (nSMI) on measures of memory and level of tau binding in the entorhinal cortices and the hippocampi. It was further hypothesized that differences in memory would be mediated by level (high/low) of binding in these neuroanatomical structures. The sample included 127 cognitively normal (CN) participants, selected from the Alzheimer’s Disease neuroimaging Initiative 3. Participants were cognitively normal, free from co-morbid disorders such as depression, and included individuals who had undergone PET imaging at baseline testing. Results found no significant differences between memory scores for SMI or nSMI participants, nor were there significant differences between groups on tau standardized uptake value ratios. There were significant main effects for tau level and location (left/right entorhinal cortices and left/right hippocampi) for the Wechsler Memory Scale-IV Logical Memory I test, and in the left entorhinal cortex for Logical Memory II. Current findings support differences in level of AV-1451 tau binding for story memory. The data provides a baseline for future researchers to utilize the cognitive measure of story memory in conjunction with tau level to develop a neuropsychological profile for individuals who may benefit from earlier intervention to slow progression of neurodegenerative decline.

Comments

Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) andDOD 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 Associatiosn; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; 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.; Lumosity; 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 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.

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