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ASU Electronic Theses and Dissertations


This collection includes most of the ASU Theses and Dissertations from 2011 to present. ASU Theses and Dissertations are available in downloadable PDF format; however, a small percentage of items are under embargo. Information about the dissertations/theses includes degree information, committee members, an abstract, supporting data or media.

In addition to the electronic theses found in the ASU Digital Repository, ASU Theses and Dissertations can be found in the ASU Library Catalog.

Dissertations and Theses granted by Arizona State University are archived and made available through a joint effort of the ASU Graduate College and the ASU Libraries. For more information or questions about this collection contact or visit the Digital Repository ETD Library Guide or contact the ASU Graduate College at gradformat@asu.edu.


Mime Type
  • application/pdf
Date Range
2012 2018


Alzheimer’s disease is a major problem affecting over 5.7 million Americans. Although much is known about the effects of this neurogenerative disease, the exact pathogenesis is still unknown. One very important characteristic of Alzheimer’s is the accumulation of beta amyloid protein which often results in plaques. To understand these beta amyloid proteins better, antibody fragments may be used to bind to these oligomers and potentially reduce the effects of Alzheimer’s disease. This thesis focused on the expression and crystallization the fragment antigen binding antibody fragment A4. A fragment antigen binding fragment was chosen to be worked with as it is …

Contributors
Colasurd, Paige, Nannenga, Brent, Mills, Jeremy, et al.
Created Date
2018

Alzheimer’s disease (AD) is characterized by the degeneration of cholinergic basal forebrain (CBF) neurons in the nucleus basalis of Meynert (nbM), which provides the majority of cholinergic input to the cortical mantle and together form the basocortical cholinergic system. Histone deacetylase (HDAC) dysregulation in the temporal lobe has been associated with neuronal degeneration during AD progression. However, whether HDAC alterations play a role in cortical and cortically-projecting cholinergic nbM neuronal degeneration during AD onset is unknown. In an effort to characterize alterations in the basocortical epigenome semi-quantitative western blotting and immunohistochemistry were utilized to evaluate HDAC and sirtuin (SIRT) levels …

Contributors
Mahady, Laura Jean, Mufson, Elliott J, Bimonte-Nelson, Heather, et al.
Created Date
2018

An in vitro model of Alzheimer’s disease (AD) is required to study the poorly understood molecular mechanisms involved in the familial and sporadic forms of the disease. Animal models have previously proven to be useful in studying familial Alzheimer’s disease (AD) by the introduction of AD related mutations in the animal genome and by the overexpression of AD related proteins. The genetics of sporadic Alzheimer’s is however too complex to model in an animal model. More recently, AD human induced pluripotent stem cells (hiPSCs) have been used to study the disease in a dish. However, AD hiPSC derived neurons do …

Contributors
Raman, Sreedevi, Brafman, David, Stabenfeldt, Sarah, et al.
Created Date
2017

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that affects 5.4 million Americans. AD leads to memory loss, changes in behavior, and death. The key hallmarks of the disease are amyloid plaques and tau tangles, consisting of amyloid-β oligomers and hyperphosphorylated tau, respectively. Rho-associated, coiled-coil-containing protein kinase (ROCK) is an enzyme that plays important roles in neuronal cells including mediating actin organization and dendritic spine morphogenesis. The ROCK inhibitor Fasudil has been shown to increase learning and working memory in aged rats, but another ROCK inhibitor, Y27632, was shown to impair learning and memory. I am interested in exploring how …

Contributors
Turk, Mari Nicole, Huentelman, Matt, Kusumi, Kenro, et al.
Created Date
2017

Alzheimer’s disease (AD), despite over a century of research, does not have a clearly defined pathogenesis for the sporadic form that makes up the majority of disease incidence. A variety of correlative risk factors have been identified, including the three isoforms of apolipoprotein E (ApoE), a cholesterol transport protein in the central nervous system. ApoE ε3 is the wild-type variant with no effect on risk. ApoE ε2, the protective and most rare variant, reduces risk of developing AD by 40%. ApoE ε4, the risk variant, increases risk by 3.2-fold and 14.9-fold for heterozygous and homozygous representation respectively. Study of these …

Contributors
Lakers, Mary Frances, Brafman, David, Haynes, Karmella, et al.
Created Date
2017

The pathophysiology of neurodegenerative diseases, such as Alzheimer’s disease (AD), remain difficult to ascertain in part because animal models fail to fully recapitulate the complex pathophysiology of these diseases. In vitro models of neurodegenerative diseases generated with patient derived human induced pluripotent stem cells (hiPSCs) and human embryonic stem cells (hESCs) could provide new insight into disease mechanisms. Although protocols to differentiate hiPSCs and hESCs to neurons have been established, standard practice relies on two dimensional (2D) cell culture systems, which do not accurately mimic the complexity and architecture of the in vivo brain microenvironment. I have developed protocols to …

Contributors
Petty, Francis John, Brafman, David, Stabenfeldt, Sarah, et al.
Created Date
2016

Vitamin D deficiency has been previously associated with a higher Alzheimer’s disease (AD) risk, a condition marked by dependent living and severe cognitive impairment. AD is histologically defined by the presence of brain amyloid beta (Aβ) plaques and neurofibrillary tangles. Ways to enhance Aβ clearance have been examined in order to sustain cognition and delay AD onset. In vitro and in vivo studies suggest that vitamin D might enhance brain Aβ transportation to the periphery by up-regulating P-glycoprotein production. The purpose of this study was to examine the effect of vitamin D supplementation on plasma Aβ in an older population. …

Contributors
Miller, Brendan Joseph, Johnston, Carol, Whisner, Corrie, et al.
Created Date
2015

Alzheimer's disease (AD) is the most common type of dementia, affecting one in nine people age 65 and older. One of the most important neuropathological characteristics of Alzheimer's disease is the aggregation and deposition of the protein beta-amyloid. Beta-amyloid is produced by proteolytic processing of the Amyloid Precursor Protein (APP). Production of beta-amyloid from APP is increased when cells are subject to stress since both APP and beta-secretase are upregulated by stress. An increased beta-amyloid level promotes aggregation of beta-amyloid into toxic species which cause an increase in reactive oxygen species (ROS) and a decrease in cell viability. Therefore reducing …

Contributors
Suryadi, Vicky Rulando, Sierks, Michael, Nielsen, David, et al.
Created Date
2014

The purpose of this study is to identify the needs of older adults with Alzheimer's disease (AD) and related dementias (ADRD) admitted to a rehabilitation setting where they are expected to physically and mentally function to their optimal level of health. To date, no studies have identified the needs and concerns of ADRD patients in rehabilitation settings. The Needs-Driven Dementia-Compromised Behavior (NDB) Model, the researcher's clinical experience, and the state of the current scientific literature will help guide the study. An exploratory qualitative research approach was employed to gather data and discover new information about the ADRD patient's needs and …

Contributors
Allen, Angela Marie, Coon, David W, McCarthy, Marianne, et al.
Created Date
2014

Alzheimer's Disease (AD) is a progressive neurodegenerative disease accounting for 50-80% of dementia cases in the country. This disease is characterized by the deposition of extracellular plaques occurring in regions of the brain important for cognitive function. A primary component of these plaques is the amyloid-beta protein. While a natively unfolded protein, amyloid-beta can misfold and aggregate generating a variety of different species including numerous different soluble oligomeric species some of which are precursors to the neurofibrillary plaques. Various of the soluble amyloid-beta oligomeric species have been shown to be toxic to cells and their presence may correlate with progression …

Contributors
Venkataraman, Lalitha, Sierks, Michael, Rege, Kaushal, et al.
Created Date
2013