Publication Date

Fall 12-3-2019


School of Health Sciences


Biology: Biomedical Sciences


Amyloid Beta, Alzheimer's, dementia, neurodegeneration, Tau, Neurofibrillary tangles, Calcium, Reactive oxygen species, ROS, Glutamate


Amino Acids, Peptides, and Proteins | Biochemistry | Cell Biology | Cognitive Neuroscience | Medical Biochemistry | Medical Cell Biology | Medical Molecular Biology | Medical Neurobiology | Molecular and Cellular Neuroscience | Molecular Biology | Nervous System Diseases | Neurology | Neurosciences


This paper reviews functions of Amyloid-β (Aβ) in healthy individuals compared to the consequences of aberrant Aβ in Alzheimer’s disease (AD). As extraneuronal Aβ accumulation and plaque formation are characteristics of AD, it is reasonable to infer a pivotal role for Aβ in AD pathogenesis. Establishing progress of the disease as well as the mechanism of neurodegeneration from AD have proven difficult (Selkoe, 1994). This thesis provides evidence suggesting the pathogenesis of AD is due to dysfunctional neuronal processes involving Aβ’s synaptic malfunction, abnormal interaction with tau, and disruption of neuronal homeostasis. Significant evidence demonstrates that AD symptoms are partially due to aberrant Aβ, and further experimental research may focus on repairing or preventing the noxious effects of Aβ.