Buch, Englisch, Band 44, 272 Seiten, Paperback, Format (B × H): 210 mm x 279 mm, Gewicht: 699 g
Buch, Englisch, Band 44, 272 Seiten, Paperback, Format (B × H): 210 mm x 279 mm, Gewicht: 699 g
Reihe: Journal of Neural Transmission. Supplementa
ISBN: 978-3-211-82549-5
Verlag: Springer Vienna
Zielgruppe
Research
Autoren/Hrsg.
Weitere Infos & Material
Primary cultures of neurons for testing neuroprotective drug effects.- Regulation of proteolytic processing of the amyloid ?-protein precursor in Alzheimer’s disease in transfected cell lines and in brain slices.- Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration.- An aggregate brain cell culture model for studying neuronal degeneration and regeneration.- The organotypic entorhinal-hippocampal complex slice culture of adolescent rats. A model to study transcellular changes in a circuit particularly vulnerable in neurodegenerative disorders.- The use of ion-sensitive electrodes and fluorescence imaging in hippocampal slices for studying pathological changes of intracellular Ca2+ regulation.- The cultured fibroblast model.- Psychometric testing in rats during normal ageing. Procedures and results.- Ultrastructural changes in brain parenchyma during normal aging and in animal models of aging.- Morphological hippocampal changes during normal aging and their relation to cognitive deterioration.- The function of the NMDA-receptor during normal brain aging.- Age-related alterations by chronic intermittent hypoxia on cerebral synaptosomal ATPase activities.- Impairment in memory function and neurodegenerative changes in the cholinergic basal forebrain system induced by chronic intake of ethanol.- Dysfunction of the brain cholinergic system during aging and after lesions of the nucleus basalis of Meynert.- Receptor function in cortical rat brain regions after lesion of nucleus basalis.- Trophic factors during normal brain aging and after functional damage.- Alzheimer’s disease and transgenic mice.- An aspect of Alzheimer neuropathology after suicide transport damage.- AF64A-induced brain damage and its relation to dementia.-Desensitization of brain insulin receptor. Effect on glucose/energy and related metabolism.