The effect of Thymosine-ß4 on macrophage phenotype in Alzheimer’s disease
Publication Date
July 19, 2019
Creator
Abstract
Background: Alzheimer’s disease (AD) is the most common form of dementia throughout the population. It is a neurodegenerative disorder in which the risk of developing the disease can increase with age. The pathology of AD is closely associated with neuroinflammation. As part of the immune response, neuroinflammation acts as a form of protection. The G-sequestering protein, Thymosin beta 4 (T4), possesses anti-inflammatory properties, and is present in abundance within macrophages. This study aimed to investigate the effect of T4 on the phenotypes of peritoneal macrophages collected from mouse models of AD. In this study, a variety of methods were used to assess the effect of T4 and LPS on macrophage phenotypes in models of AD. These include the collection and isolation of peritoneal macrophages, cell culture, macrophage and antibody treatment, flow cytometry analysis and the corresponding statistics to represent data graphically. The results obtained show that there were minimal effects of T4 on the expression of the M1 (CD80) and M2 (CD23) macrophage phenotypes in AD. Therefore, a more definitive role for the effects of T4 on macrophage phenotypes was not achieved.
Item Type
ethesis
Thesis Type
MRes
Supervisors
Subjects (LC)
Associated Schools / Departments
School of Life Sciences
eprints ID
56634
UoN Repository URI
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Name
Thesis Ikra Hussain.pdf
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Full-text
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Examined
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3.39 MB
Format
Adobe PDF
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