Open Access. Powered by Scholars. Published by Universities.®
Articles 1 - 3 of 3
Full-Text Articles in Entire DC Network
The Regulation Of Extracellular Amyloid-Β Levels By Ionotropic Glutamatergic Transmission In An Alzheimer’S Disease Mouse Model, Jane Cecelia Hettinger
The Regulation Of Extracellular Amyloid-Β Levels By Ionotropic Glutamatergic Transmission In An Alzheimer’S Disease Mouse Model, Jane Cecelia Hettinger
Arts & Sciences Electronic Theses and Dissertations
Brain extracellular concentration of the peptide amyloid-β (Aβ) is a major contributor to Alzheimer’s disease (AD) pathogenesis. High Aβ levels in the extracellular space precipitate aggregation of the peptide into soluble and insoluble toxic species. This process begins decades before cognitive impairment and triggers the cascade of pathology that eventually leads to AD. Synaptic activity is key to the regulation of extracellular Aβ levels. Presynaptic activity drives the production of Aβ, while postsynaptic receptor activation exhibits more nuanced regulation. For example, high levels of NMDA receptor (NMDA-R) activation have been shown to decrease Aβ production through the extracellular signal-regulated kinase …
Characterization Of Neuronal Specific Responses To Induced Misfolded Protein Stress In Caenorhabditis Elegans, Claire Gormley
Characterization Of Neuronal Specific Responses To Induced Misfolded Protein Stress In Caenorhabditis Elegans, Claire Gormley
Senior Honors Projects, 2010-2019
Abstract
Misfolded protein stress has been associated with many types of disease,
including neurodegenerative disorders like Alzheimer’s, Parkinson’s and Huntington’s
disease. When a cell accumulates misfolded proteins in the endoplasmic reticulum,
misfolded protein stress occurs and the unfolded protein response (UPR) is triggered to
induce mechanisms that will allow the cell to either survive or undergo cell death. The
nascent polypeptide associated complex (NAC) is a co-translational chaperone and α/β
heterodimer that manages protein folding and localization, and protects against misfolded
protein stress; changes in NAC function have been linked to both neurodegeneration and
cancer. In these studies, I depleted …
4-Nonylphenol Induces Neurodegeneration By Altering Cytoskeleton, Cynthia Carreon
4-Nonylphenol Induces Neurodegeneration By Altering Cytoskeleton, Cynthia Carreon
Open Access Theses & Dissertations
4-nonylphenol (4-NP), an endocrine-disrupting compound (EDC), has been shown to affect brain development and may cause neurodegeneration. In the environment, 4-NP arises as a degradation product of alkylphenol polyethoxylates, compounds widely used as nonionic surfactants in commercial production, as well as in herbicides, pesticides, polystyrene plastics, and paints and has been shown to undergo a high level of accumulation in biological tissues. However, the mechanism by which 4-NP exerts its effect is not understood. Recent results from our laboratory indicate that Gβγ, an important component of the G protein-signaling pathway, induces neuronal outgrowth and differentiation by modulating microtubule (MT) assembly, …