Life Sciences Commons^™

Biophysical Characterization And Cross-Seeding Properties Of Lfaos, Novel Prion-Like Oligomers Of The Amyloid-Beta Peptide Involved In Alzheimer’S Disease, Morgan C. Woodrow

Honors Theses

The amyloid-beta (Aβ) protein is known to play an important role in the etiology of Alzheimer’s disease (AD). Aβ peptide aggregates in the brains of AD patients to form soluble oligomers as well as insoluble fibrils. Oligomers of Aβ are now known to be the primary toxic agents in AD. Evidence is beginning to emerge regarding a conserved prion-like propagation mechanism in AD. One of the principal characteristics of prion diseases is their ability to self-propagate via a template-assisted-corruptive mechanism. Our lab has previously characterized a unique ‘Aβ prion’ called Large Fatty-Acid- Derived Oligomers (LFAOs). This project examines the ability …

Exploring The Interactions Between Interleukin-8 (Il8) And Amyloid-Β (Aβ) Peptide In Traumatic Brain Injury, Olivia G. Gibson

Honors Theses

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive dysfunction and memory loss, and pathologically characterized by amyloid-beta (Aβ) plaques and inflammation. Recent research has shown that these Aβ plaques are also found in traumatic

brain injury (TBI) patients. This discovery has led to a proposed pathway leading from traumatic brain injuries to dementia, more specifically AD. After a TBI, human granulin-A (GRN) and interleukin-8 (IL8) are released and the number of elastases in the brain increases in response to the inflammation response. IL8 is a cytokine that is released in acute inflammation responses, and the levels of IL8 …

Exploring The Interaction Between Human Granulin-A (Hgrn-A) And Amyloid-Β (Aβ) Peptide, Michael Samel

Honors Theses

Alzheimer’s disease (AD) is the most common form of dementia affecting people over the age of 60, yet a detailed understanding of the molecular changes involved in AD remains a significant challenge to modern medicine. The hallmarks of an AD brain include the presence of senile plaques formed by a protein called amyloid-β (Aβ), along with inflammation of the brain. Aβ self-associates to form clumps of protein called “aggregates” which are known to be the primary toxic agents in AD pathology; however, several other proteins have also been implicated in this pathology. One such protein called progranulin (PGRN), which under …