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Full-Text Articles in Diseases
A Role Of Vitamin B2 In Reducing Amyloid-Beta Toxicity In A Caenorhabditis Elegans Alzheimer’S Disease Model, Muhammad Tukur Ameen
A Role Of Vitamin B2 In Reducing Amyloid-Beta Toxicity In A Caenorhabditis Elegans Alzheimer’S Disease Model, Muhammad Tukur Ameen
Electronic Theses and Dissertations
Alzheimer’s disease (AD) is associated with amyloid-beta peptide deposition and loss of mitochondrial function. Using a transgenic C. elegans AD worm model expressing amyloid-beta in body wall muscle, we determined that supplementation with either of the forms of vitamin B2, flavin mononucleotide (FMN) or flavin adenine dinucleotide (FAD) protected against amyloid-beta mediated paralysis. FMN and FAD were then assayed to determine effects on ATP, oxygen consumption, and reactive oxygen species (ROS) with these compounds not significantly improving any of these mitochondrial bioenergetic functions. Knockdown of the daf-16/FOXO transcriptional regulator or the FAD synthase enzyme completely abrogated the …
Is Detection Of Preclinical Alzheimer’S Disease Possible?, Shana Brawer
Is Detection Of Preclinical Alzheimer’S Disease Possible?, Shana Brawer
The Science Journal of the Lander College of Arts and Sciences
No abstract provided.
Chlamydia Pneumoniae: An Etiologic Agent For Late-Onset Dementia, Brian J. Balin Phd, Christine Hammond, Christopher S. Little, Susan Hingley, Zein Al-Atrache, Denah Appelt, Judith A Whittum-Hudson, Alan P Hudson
Chlamydia Pneumoniae: An Etiologic Agent For Late-Onset Dementia, Brian J. Balin Phd, Christine Hammond, Christopher S. Little, Susan Hingley, Zein Al-Atrache, Denah Appelt, Judith A Whittum-Hudson, Alan P Hudson
PCOM Scholarly Papers
The disease known as late-onset Alzheimer's disease is a neurodegenerative condition recognized as the single most common form of senile dementia. The condition is sporadic and has been attributed to neuronal damage and loss, both of which have been linked to the accumulation of protein deposits in the brain. Significant progress has been made over the past two decades regarding our overall understanding of the apparently pathogenic entities that arise in the affected brain, both for early-onset disease, which constitutes approximately 5% of all cases, as well as late-onset disease, which constitutes the remainder of cases. Observable neuropathology includes: neurofibrillary …