Beta-Amyloid Inhibition of Alpha 7 Nicotinic Acetylcholine Receptors and Factors That Potentially Influence the Aβ/nAChR Interaction

Citation data:

Brigham Young University - Provo

Publication Year:
2013
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Downloads 98
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Repository URL:
https://scholarsarchive.byu.edu/etd/4179; https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5178&context=etd
Author(s):
Jacobsen, Christopher L.
Publisher(s):
Brigham Young University - Provo
Tags:
Alzheimer's disease; nAChR; beta-amyloid; Congo Red; antibiotics; Cell and Developmental Biology; Physiology
thesis / dissertation description
Alzheimer's disease (AD) is a neurodegenerative disorder that manifests in the form of deficiencies in cognitive processes such as memory and learning. The pathological features of AD include hyperphosphorylated tau proteins that form neurofibrillary tangles as well as senile plaques composed primarily of the peptide β-amyloid (Aβ). When present in high concentrations in the brain, Aβ inhibits certain subtypes of neuronal nicotinic acetylcholine receptors (nAChRs) in the hippocampus. The effects of Aβ in the hippocampus have proven to be neurotoxic, resulting in reduced functionality of nAChRs and the subsequent death of neurons in the cholinergic pathway. The early stages of AD are characterized by reduction of nAChR density and by degeneration of the cholinergic neurons that provide input to the hippocampus. Because the hippocampus plays a critical role in memory formation and other cognitive processes, dysfunction in this brain region results in significant cognitive deficiencies. Understanding the interaction between Aβ and the structurally and functionally diverse nAChR subtypes and possible downstream effects in signaling cascades that might result from that interaction are important steps in comprehending AD pathogenesis. Comprehension of this interaction and factors that might influence it could lead to the development of pharmaceutical agents useful in the treatment of AD.