caa a22 4500 477038220 CHVBK 20180405111310.0 cr unu---uuuuu 170330e19960601xx s 000 0 eng 10.1007/BF02755589 doi (NATIONALLICENCE)springer-10.1007/BF02755589 Amyloid β-peptide and oxidative cellular injury in Alzheimer's disease [Elektronische Daten] [Robert Mark, Emmanuelle Blanc, Mark Mattson] Alzheimer's disease is a progressive neurodegenerative disorder that affects primarily learning and memory functions. There is significant neuronal loss and impairment of metabolic functioning in the temporal lobe, an area believed to be crucial for learning and memory tasks. Aggregated deposits of amyloid β-peptide may have a causative role in the development and progression of AD. We review the cellular actions of Aβ and how they can contribute to the cytotoxicity observed in AD. Aβ causes plasma membrane lipid peroxidation, impairment of ionmotive ATPases, glutamate uptake, uncoupling of a G-protein linked receptor, and generation of reactive oxygen species. These effects contribute to the loss of intracellular calcium homeostasis reported in cultured neurons. Many cell types other than neurons show alterations in the Alzheimer's brain. The effects of Aβ on these cell types is also reviewed. Humana Press Inc, 1996 Excitotoxicity nationallicence nerve nationallicence astrocyte nationallicence microglia nationallicence endothelial cell nationallicence ion-motive ATPase nationallicence free radical nationallicence signal transduction nationallicence Mark Robert Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut Blanc Emmanuelle Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut Mattson Mark Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut Molecular Neurobiology Humana Press 12/3(1996-06-01), 211-224 0893-7648 12:3<211 1996 12 12035 https://doi.org/10.1007/BF02755589 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02755589 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Mark Robert Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut NATIONALLICENCE 700 1- Blanc Emmanuelle Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut NATIONALLICENCE 700 1- Mattson Mark Sanders-Brown Research Center on Aging and Department of Anatomy & Neurobiology, University of Kentucky, 40536, Lexington, KY aut NATIONALLICENCE 773 0- Molecular Neurobiology Humana Press 12/3(1996-06-01), 211-224 0893-7648 12:3<211 1996 12 12035 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer