Open Access. Powered by Scholars. Published by Universities.®

Biochemistry Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 3 of 3

Full-Text Articles in Biochemistry

Investigation Of Alzheimer’S Amyloid-Β Protein Aggregation With A New Fluorescent Dye., Emma Alberty Jan 2024

Investigation Of Alzheimer’S Amyloid-Β Protein Aggregation With A New Fluorescent Dye., Emma Alberty

Undergraduate Research Symposium

Alzheimer’s Disease (AD) is the most common form of dementia characterized by the impairment of at least two brain functions such as memory loss and judgement. AD is a progressive illness that can last as many as 20 years. AD is largely considered to be caused by the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. A better understanding of the structure and function of these plaques may lead to clearer understanding of the disease. To analyze amyloid plaques, aggregation assays are often used. During these assays we begin with monomer and place the sample in biological conditions to …


Alzheimer's And Amyloid Beta: Amyloidogenicity And Tauopathy Via Dyshomeostatic Interactions Of Amyloid Beta, Jordan Tillinghast Dec 2019

Alzheimer's And Amyloid Beta: Amyloidogenicity And Tauopathy Via Dyshomeostatic Interactions Of Amyloid Beta, Jordan Tillinghast

Senior Honors Theses

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 …


Mechanisms To Mitigate Neurodegeneration By Maintaining Mitochondrial Health, Parijat Kabiraj Jan 2014

Mechanisms To Mitigate Neurodegeneration By Maintaining Mitochondrial Health, Parijat Kabiraj

Open Access Theses & Dissertations

Cerebral accumulation of amyloidogenic protein aggregates is most frequently observed in the pathogenesis of neurodegenerative diseases. Recent studies showed prion like spreading of beta amyloid (A beta) in Alzheimer's disease (AD) and alpha synuclein protein in Parkinson's disease (PD) brain. Failure or compromise to the chaperone activity of protein disulfide isomerase (PDI) is also been reported as a major factor of aggregate formation. Nitrosative stress mediated S-nitrosylation (SNO) of protein disulfide isomerase (PDI), a housekeeping oxidoreductase, has been implicated in the pathogenesis of sporadic PD and AD. Mitochondrial dysfunction, leading to elevated levels of reactive oxygen species (ROS), is associated …