Alzheimer’s disease (AD) is a neurodegenerative disease with characteristic amyloid, neurofibrillary tangles, and neuronal death in the brain. The major component of amyloid is monomeric amyloid beta (Aβ) protein, as well as its oligomers and large fibrils. Aβ, especially oligomeric Aβ, causes neurotoxicity. The aim of the present study was to investigate how Aβ is metabolized in the presence of microglia cells. We have used a cellular model to study the phagocytosis and degradation of Aβ by BV-2, a murine microglia cell line. We also examined if amylin, a pancreatic peptide, influences the metabolism of Aβ by BV-2 cells. Through Western blot analysis, we observed the phagocytosis of Aβ by BV-2 cells. In our investigation of the role of amylin, we observed a trend in our finding that amylin increased phagocytosis in BV-2 cells and decreased aggregation in the culture medium. Our data demonstrate that amylin may modulate microglia function in the AD brain and has potential to become therapeutic for the disease.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/26672 |
| Date | 02 November 2017 |
| Creators | Leung, Lorene Chung |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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