First Advisor

Philip Copenhaver

Date of Award

Summer 8-8-2024

Document Type

Thesis

Degree Name

Bachelor of Science (B.S.) in Biology and University Honors

Department

Biology

Language

English

Subjects

Alzheimer's Disease, neurodegeneration, amyloid hypothesis, antibody therapies, alternative models

DOI

10.15760/honors.1593

Abstract

Alzheimer's Disease (AD) is the leading cause of dementia worldwide. Patients with this condition first experience mild cognitive impairment, followed by the loss of memory, cognitive skills, identity, and the ability to perform daily tasks unassisted, eventually culminating in death.

The dominant hypothesis for the mechanism of Alzheimer's, the amyloid cascade hypothesis, based on early-onset AD, suggests that amyloid plaques formed by Aβ peptides cause a cascading effect involving an increase in toxic tau protein, which is correlated with the disease progression of Alzheimer's patients. While the mechanism of late sporadic AD is not fully understood, this has been used as a framework to develop drug therapies. These therapies did not prove effective until the recent development of several monoclonal antibody therapy drugs which mark amyloid plaques for destruction by microglial cells. However, there can be serious side effects to these drugs, including bleeding and inflammation in the brain. This paper will discuss the state of research on antibody therapies and the relevance of the amyloid cascade hypothesis in Alzheimer's research. There are alternative and supplemental hypotheses to the amyloid cascade hypothesis, which may change the perception of antibody therapies. Finally, I will discuss the implications of these therapies on Alzheimer's research and patient outcomes.

Persistent Identifier

https://archives.pdx.edu/ds/psu/42411

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