Date of Award

Spring 2021

Degree Name

Bachelor of Science

Department

Biology; College of Arts & Sciences

First Advisor

Megan Wright

Abstract

More than 6 million people in America are living with Alzheimer’s Disease (AD) and there are currently no cures or treatments. It is time to move on from the ꞵ-amyloid hypothesis and broaden AD research. New research is suggesting that dietary exposure to a cyanobacterial toxin known as L-BMAA is causing neurodegenerative diseases such as AD, Amyotrophic lateral sclerosis (ALS), and Parkinson’s Disease. L-BMAA is misincorporated during protein folding, in place of the proper amino acid, L-Serine. It has been shown that the naturally occurring amino acid, L-Serine, can provide neuroprotection against L-BMAA, but the mechanism by which L-Serine infers this protection is unclear. This thesis will examine how the amino acid L-Serine can be used as a preventative measure against L-BMAA Induced Alzheimer’s Disease. Both articles by Dunlop et al., 2018 have shown that L-Serine provides neuroprotection by diluting the cell and decreasing the probability that L-BMAA is misincorporated, and also by increasing the unfolded protein response. In both studies, QPCR and Western Blotting were used to determine what genes and cellular pathways both L-Serine and L-BMAA activated. As more researchers begin to move away from the ꞵ-amyloid hypothesis, it is important that we broaden our research horizons and work with other disciplines within the scientific community. By studying AD from different angles, a better understanding of AD will be gained, potentially offering other therapeutic approaches to treating AD.

Additional Files

BIO CiminoJ poster.pdf (959 kB)

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How The Amino Acid L-Serine Provides Neuroprotection Against L-BMAA Induced Alzheimer’s Disease

More than 6 million people in America are living with Alzheimer’s Disease (AD) and there are currently no cures or treatments. It is time to move on from the ꞵ-amyloid hypothesis and broaden AD research. New research is suggesting that dietary exposure to a cyanobacterial toxin known as L-BMAA is causing neurodegenerative diseases such as AD, Amyotrophic lateral sclerosis (ALS), and Parkinson’s Disease. L-BMAA is misincorporated during protein folding, in place of the proper amino acid, L-Serine. It has been shown that the naturally occurring amino acid, L-Serine, can provide neuroprotection against L-BMAA, but the mechanism by which L-Serine infers this protection is unclear. This thesis will examine how the amino acid L-Serine can be used as a preventative measure against L-BMAA Induced Alzheimer’s Disease. Both articles by Dunlop et al., 2018 have shown that L-Serine provides neuroprotection by diluting the cell and decreasing the probability that L-BMAA is misincorporated, and also by increasing the unfolded protein response. In both studies, QPCR and Western Blotting were used to determine what genes and cellular pathways both L-Serine and L-BMAA activated. As more researchers begin to move away from the ꞵ-amyloid hypothesis, it is important that we broaden our research horizons and work with other disciplines within the scientific community. By studying AD from different angles, a better understanding of AD will be gained, potentially offering other therapeutic approaches to treating AD.