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Interactions Between Amyloid-Beta And Microglial Cells, Lisa Gouwens
Interactions Between Amyloid-Beta And Microglial Cells, Lisa Gouwens
Dissertations
Alzheimer’s disease (AD), the most common cause of dementia, is a neurodegenerative condition characterized by loss of memory and intellectual abilities. Intracellular plaques of aggregated amyloid-beta (Ab) protein are a well-known pathology associated with AD. Although symptoms usually appear late in life, the accumulation of Ab begins decades earlier and causes activation of microglia, the brain’s immune cells. The ensuing inflammation contributes significantly to neurodegeneration. Determination of the particular form of Ab that causes the most damage in the brain is one of the major questions in the AD field. My research focused on the interactions of microglia with monomers, …
Soluble Amyloid-Beta 42 Aggregates Stimulate Cellular Inflammation Independent Of Cd47, Sanjib Karki
Soluble Amyloid-Beta 42 Aggregates Stimulate Cellular Inflammation Independent Of Cd47, Sanjib Karki
Dissertations
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the accumulation and deposition of aggregated amyloid-β protein (Aβ). Most of the studies indicate that Aβ1-42) and Aβ(1-40) play an important role in the neurodegenerative pathology in AD. A critical component of AD pathology is inflammation, which results from the activation of glial cells around the Aβ deposits. The goal of my dissertation research was to determine the role of Aβ aggregation in microglia-triggered inflammation and identify cellular components that mediate the inflammatory response. CD47 is a cellular receptor found on the microglia surface and it has been proposed to have …
Microglial Activation By Amyloid-Beta, Geeta Subhash Paranjape
Microglial Activation By Amyloid-Beta, Geeta Subhash Paranjape
Dissertations
Paranjape, Geeta S.,Ph.D.,University of Missouri-Saint Louis, May 2012. Aβ(1-42) Protofibrils But Not Fibrils Activate Microglia. Major Professor: Michael R. Nichols. One of the hallmark features of the Alzheimer’s disease (AD) brain is the extracellular deposition of amyloid-β protein (Aβ) in both fibrillar (senile plaques) and diffuse forms. Significant proinflammatory markers including activated microglia and cytokines have been detected surrounding the plaques but are absent in diffuse areas suggesting that microglial activation is sensitive to Aβ structure. Since Aβ displays structural polymorphism in vitro, we sought to determine the relationship between Aβ aggregation state and microglial proinflammatory response. Size exclusion chromatography …
Role Of Amyloid Beta Assembly State In The Human Immune Response, Deepa Viswanathan
Role Of Amyloid Beta Assembly State In The Human Immune Response, Deepa Viswanathan
Dissertations
Alzheimer’s disease (AD) is a slowly progressing neurodegenerative disease that leads to dementia. Histopathological hallmarks that characterize AD are senile plaques formed by extracellular deposition of Amyloid beta (Aβ) peptide and intracellular aggregates of hyperphosphorylated tau protein. The plaques, which are found in the brain parenchyma, comprise both 40 and 42 residue Aβ. Aggregation of Aβ is an established pathogenic mechanism in AD, but little is known about the initiation of this process in vivo. Several studies have revealed significant inflammatory markers such as activated microglia and cytokines surrounding the plaques. Plaques are a hallmark of AD, but they are …
Activation Of The Innate Immune Response By The Alzheimer's Amyloid Beta Protein Via Toll-Like Receptors, Udan Lourdes Maria
Activation Of The Innate Immune Response By The Alzheimer's Amyloid Beta Protein Via Toll-Like Receptors, Udan Lourdes Maria
Dissertations
Alzheimer’s Disease (AD) is the most common form of neurodegenerative disease characterized by the generation and deposition of amyloid beta plaques and the formation of neurofibrillary tangles. A wealth of data now demonstrate that inflammation is a prominent feature in AD pathology and a potential therapeutic target for the treatment and prevention of the disease. The emergence of evidence linking amyloid beta protein (Aβ), the primary component of senile plaques, to inflammation has led to new insights into understanding AD pathology. Aβ, a protein fragment resulting from cleavage of human amyloid precursor protein (APP), primarily exists in two forms: a …