Data on Alzheimer Disease Detailed by Researchers at University of Kentucky (Oxidative Stress, Amyloid-b Peptide, and Altered Key Molecular Pathways…

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Data on Alzheimer Disease Detailed by Researchers at University of Kentucky (Oxidative Stress, Amyloid-b Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease)

By a News Reporter-Staff News Editor at Pain & Central Nervous System Week -- Data detailed on Neurodegenerative Diseases and Conditions - Alzheimer Disease have been presented. According to news reporting out of Lexington, Kentucky, by NewsRx editors, research stated, "Oxidative stress is implicated in the pathogenesis and progression of Alzheimer's disease (AD) and its earlier stage, amnestic mild cognitive impairment (aMCI). One source of oxidative stress in AD and aMCI brains is that associated with amyloid-b peptide, Ab1-42 oligomers."

Our news journalists obtained a quote from the research from the University of Kentucky, "Our laboratory first showed in AD elevated oxidative stress occurred in brain regions rich in Ab1-42, but not in Ab1-42-poor regions, and was among the first to demonstrate Ab peptides led to lipid peroxidation (indexed by HNE) in AD and aMCI brains. Oxidatively modified proteins have decreased function and contribute to damaged key biochemical and metabolic pathways in which these proteins normally play a role. Identification of oxidatively modified brain proteins by the methods of redox proteomics was pioneered in the Butterfield laboratory. Four recurring altered pathways secondary to oxidative damage in brain from persons with AD, aMCI, or Down syndrome with AD are interrelated and contribute to neuronal death. This 'Quadrilateral of Neuronal Death' includes altered: glucose metabolism, mTOR activation, proteostasis network, and protein phosphorylation. Some of these pathways are altered even in brains of persons with preclinical AD. We opine that targeting these pathways pharmacologically and with lifestyle changes potentially may provide strategies to slow or perhaps one day, prevent, progression or development of this devastating dementing disorder."

According to the news editors, the research concluded: "This invited review outlines both in vitro and in vivo studies from the Butterfield laboratory related to Ab1-42 and AD and discusses the importance and implications of some of the major achievements of the Butterfield laboratory in AD research."

For more information on this research see: Oxidative Stress, Amyloid-b Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease. Journal of Alzheimer's Disease, 2018;62(3):1345-1367. Journal of Alzheimer's Disease can be contacted at: IOS Press, Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands (see also Neurodegenerative Diseases and Conditions - Alzheimer Disease).

Our news journalists report that additional information may be obtained by contacting D.A. Butterfield, Dept. of Chemistry and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, United States.

The direct object identifier (DOI) for that additional information is: https://doi.org/10.3233/JAD-170543. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

Publisher contact information for the Journal of Alzheimer's Disease is: IOS Press, Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands.

Keywords for this news article include: Amyloid, Kentucky, Dementia, Lexington, Tauopathies, United States, Alzheimer Disease, Health and Medicine, Peptides and Proteins, North and Central America, Brain Diseases and Conditions, Neurodegenerative Diseases and Conditions, Central Nervous System Diseases and Conditions.