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
Tillinghast, Jordan, "Alzheimer's and Amyloid Beta: Amyloidogenicity and Tauopathy via Dyshomeostatic Interactions of Amyloid Beta" (2019). Senior Honors Theses. 918.
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.
Amino Acids, Peptides, and Proteins Commons, Biochemistry Commons, Cell Biology Commons, Cognitive Neuroscience Commons, Medical Biochemistry Commons, Medical Cell Biology Commons, Medical Molecular Biology Commons, Medical Neurobiology Commons, Molecular and Cellular Neuroscience Commons, Molecular Biology Commons, Nervous System Diseases Commons, Neurology Commons, Neurosciences Commons