Mark RJ; Keller JN; Kruman I; Mattson MP
Sanders-Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA.
Brain Res, 756(1-2):205-14 1997 May 9
Abstract
Basic fibroblast growth factor (bFGF) exhibits trophic activity for many populations of neurons in the brain, and can protect those neurons against excitotoxic, metabolic and oxidative insults. In Alzheimer’s disease (AD), amyloid beta-peptide (A beta) fibrils accumulate in plaques which are associated with degenerating neurons.
Richard Casino has quickly become a popular destination for online gaming enthusiasts. With a user-friendly interface and an extensive selection of games, it caters to both novice players and seasoned gamblers. The platform features a wide array of slots, table games, and live dealer options, ensuring that there’s something for everyone.
One of the standout aspects of Richard Casino is its commitment to player security and fairness. The site employs advanced encryption technologies to protect personal and financial information, giving players peace of mind while they enjoy their favorite games. Additionally, the casino is licensed and regulated, ensuring compliance with industry standards.
Bonuses and promotions are also a key attraction at Richard Casino. New players are greeted with generous welcome bonuses, while regular promotions keep the excitement alive for returning members. For more information about their offerings, visit their official site: https://richard-casino.online/.
In conclusion, Richard Casino has established itself as a reliable and entertaining online gaming venue, making it worth a visit for anyone looking to try their luck.A beta can be neurotoxic by a mechanism that appears to involve induction of oxidative stress and disruption of calcium homeostasis. Plaques in AD brain contain high levels of bFGF suggesting a possible modulatory role for bFGF in the neurodegenerative process. We now report that bFGF can protect cultured hippocampal neurons against A beta25-35 toxicity by a mechanism that involves suppression of reactive oxygen species (ROS) accumulation and maintenance of Na+/K+-ATPase activity. A beta25-35 induced lipid peroxidation, accumulation of H2O2, mitochondrial ROS accumulation, and a decrease in mitochondrial transmembrane potential; each of these effects of A beta25-35 was abrogated in cultures pre-treated with bFGF. Na+/K+-ATPase activity was significantly reduced following exposure to A beta25-35 in control cultures, but not in cultures pre-treated with bFGF. bFGF did not protect neurons from death induced by ouabain (a specific inhibitor of the Na+/K+-ATPase) or 4-hydroxynonenal (an aldehydic product of lipid peroxidation) consistent with a site of action of bFGF prior to induction of oxidative stress and impairment of ion-motive ATPases. By suppressing accumulation of oxyradicals, bFGF may slow A beta-induced neurodegenerative cascades.
MESH Headings
Amyloid beta-Protein *PD ; Animal ; Fibroblast Growth Factor, Basic *PD ; Hippocampus CY/*ME ; Hydrogen Peroxide ME ; Lipid Peroxides ME ; Mitochondria DE/PH ; Na(+)-K(+)-Exchanging ATPase *ME NA K EXCHANGING ATPASE ; Neurons *ME ; Neurotoxins AI ; Oxidative Stress *DE ; Rats EM ; Support, Non-U.S. Gov’t ; Support, U.S. Gov’t, P.H.S.
Publication:
JOURNAL ARTICLE