Exposing Amyloid Beta 1-42 to neurons causes cell death. When carbonic anhydrase inhibitors (e.g. methazolamide or acetazolamide) are introduced along with 1-42 in a similar experiment, cell apoptosis is disrupted. However, when non-CA inhibitors are tested, (e.g. the indole derivative melatonin), the same disruption occurs. Are these carbonic anhydrase inhibitors acting on the same or a different pathway? One way to study the molecular mechanisms of these small molecule inhibitors is to modify their chemical structure. In this sense, when acetazolamide is methylated, apoptosis is resumed (Fossati et al., 2016). Finding a way to create N-methyl acetazolamide and N-methyl methazolamide through methylation procedures will lead to a better understanding of the pathways involved in neuronal apoptosis triggered by the Abeta peptide.
| Identifer | oai:union.ndltd.org:CLAREMONT/oai:scholarship.claremont.edu:cmc_theses-3052 |
| Date | 01 January 2018 |
| Creators | Ahn, Christopher |
| Publisher | Scholarship @ Claremont |
| Source Sets | Claremont Colleges |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | CMC Senior Theses |
| Rights | default |
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