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140122 ||| eng |
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|a 9781461534327
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| 100 |
1 |
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|a Meyer, Edwin M.
|e [editor]
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| 245 |
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|a Treatment of Dementias
|h Elektronische Ressource
|b A New Generation of Progress
|c edited by Edwin M. Meyer, James W. Simpkins, Jyunji Yamamoto, Fulton T. Crews
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| 250 |
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|a 1st ed. 1992
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| 260 |
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|a New York, NY
|b Springer US
|c 1992, 1992
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| 300 |
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|a 448 p. 31 illus
|b online resource
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| 505 |
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|a Cellular Mechanisms for Nimodipine’s Reduction of Aging-related Learning Deficits -- Selective Alterations in n-methyl-d-aspartate Receptor Coupled. Responses with Aging:Implications for Therapy -- Modulation of Frontal Cortical Acetylcholine Release by Benzodiazepine Receptor Ligands:Age-dependent Effects and Behavioral Correlates -- Section V. CNS Targeted Drug Delivery -- Enhanced Brain Delivery of Amino Acids and Peptides Through the Use of Redox Trageting Systems -- Brain Targeted Delivery of Neurotransmitters:Use of a Redox Based Chemical Delivery Stystem -- Procedures for Penetrating the Blood-brain-barrier:Studies of g-aminobutyric Acic (GABA) -- Sendai Virosome Envelopes for the Infusion of Macromolecules into Brain Neurons and Glia -- Section VI. Normal Aging -- Oxidative Stress and the Loss of Muscarinic and Dopaminergic Responsiveness in Senescence -- Unique Aspects of Muscarinic Receptor Stimulated Inositol Polyphosphate Formation in Brain:Changes in Senescence --
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| 505 |
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|a Section I. Cholinergic Drugs in Alzheimer’s Treatment -- Muscarinic Receptors:Molecular Biology and Neuropsychopharmacology -- Cholinomimetic Replacement of Cholinergic Function in Alzheimer Disease -- The Muscarinic Modulation of Acetylcholine Release from the Rat:Nostriatum Changes with Senescence -- Effects of Cholinergic Agents and Basal Forebrain Lesions in Rabbits -- Differential Effect of Aging on Hippocampal Pyramidal Cell Responses to Muscarine and Nicotine -- Modulation of Learning and Memory via Benzodiazepine Receptors:Potential Treatments for Age-related Dementia -- Acetylcholine-somatostatin Interactions:Potential Implications for the Treatment of Alzheimer’s Disease -- Section II. Growth Factors in Alzheimer’s Treatment -- The Role of Neurotrophins in the Central Nervous System:Significance for the Treatment of Neurodegenerative Diseases -- Contrasting Effects of Specific Lymphokines on the Survival of Hippocampal Neurons in Culture --
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| 505 |
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|a Growth Factor Regulation of Brain Protease Inhibitors -- Regulation of the Choline Acetyltransferase Gene -- Recombinant Human Nerve Growth Factor Increases Presynaptic Cholinergic Function Following Neuronal Damage:Implications for the Treatment of Alzheimer’s Disease -- Delayed Neuronal Death of Hippocampus (CA1) after Transient Global Ischemia:Does Nerve Growth Factor Protect Neurons Against “Killer Proteins?” -- Seizure-dependent Regulation of BDNF mRNA in the Rat Brain -- Section III. Phospholipids in Alzheimer’s Treatment -- Phosphatidylserine Stimulation of Macrophage Protein Secretion:Potential Healing and Trophic Mechanisms -- Pharmacological Effects of Phosphatidylserine in the Aging Rat Brain -- Effects of Phosphatidylserine in Age-associated Memory Impairment and Alzheimer’s Disease -- Section IV. Ion ChannelModulators in Alzheimer’s Disease -- Nimodipine Improves Learning and Sensorimotor Behaviors in Aging Mammals --
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| 505 |
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|a Role of Aluminum and Iron in Brain Disorders -- RNA Metabolism in Human Brain During Aging and in Alzheimer’s Disease:RNA Synthesis in the Nuclei Isolated from Postmortem Brain Tissue -- Regulation of Glutamate Release in Aging -- Potential Therapeutic Use of Growth Hormone in the Metabolic Treatment of Alzheimer’s Disease -- Disturbed Body Weight Control in Geriatric Rats:A Model for Anorexia in Alzheimer’s -- Section VII. Animal Models for Alzheimer’s Disease -- Cholinergic Phenotype of Septal Cell Lines -- Selective Death of Cholinergic Septohippocampal Neurons Induced by Colchicine:The Role of Axoplasmic Transport -- Inhibition of Cytochrome Oxidase Impairs Learning and HippocampalPlasticity:A Novel Animal Model of Alzheimer’s Disease -- ß-Amyloid Peptides, Aluminum and Albumin -- Transmission Study of Neurofilament Pathology in Hamster Brain Produced by Alzheimer Buffy Coat Inoculation
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| 653 |
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|a Nervous system / Surgery
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| 653 |
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|a Neuroscience
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| 653 |
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|a Neurosurgery
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| 653 |
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|a Neurosciences
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| 653 |
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|a Neurology
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| 653 |
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|a Neurology
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| 653 |
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|a Psychiatry
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| 653 |
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|a Pharmacology
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| 700 |
1 |
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|a Simpkins, James W.
|e [editor]
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| 700 |
1 |
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|a Yamamoto, Jyunji
|e [editor]
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| 700 |
1 |
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|a Crews, Fulton T.
|e [editor]
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| 041 |
0 |
7 |
|a eng
|2 ISO 639-2
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| 989 |
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|b SBA
|a Springer Book Archives -2004
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| 490 |
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|a Advances in Behavioral Biology
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| 028 |
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|a 10.1007/978-1-4615-3432-7
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| 856 |
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|u https://doi.org/10.1007/978-1-4615-3432-7?nosfx=y
|x Verlag
|3 Volltext
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| 082 |
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|a 616.8
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| 520 |
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|a Alzheimer's disease is one the foremost health problems facing every society fortunate enough to attain a level of medical care that ensures an average lifespan of over 70 years of age. The cause of the disease remains unknown, and no single therapeutic approach has yet been found highly efficacious. Indeed, as the complexity of its effects on brain neuronal systems becomes elucidated, the concept emerges that Alzheimer's disease may be an umbrella term for multiple Alzheimer's-type syndromes that can be differentiated based on etiology (hereditary versus sporadic), neurochemical deficits, and extent of pathology. Whether one or more disease processes is involved, it seems increasingly unlikely that any single drug will provide efficacious relief across the broad spectrum of symptoms reflected in large subject populations. Rational therapeutic approaches may yield long term amelioration of many symptoms in selected groups of patients; and individual symptoms may be ameliorated in larger populations. Multiple approaches may be combined to optimize therapeutic effects. For example, a variety of approaches remain focused on restoration of cholinergic neurodegeneration and enhancing cholinergic neurotransmission, whereas other approaches attempt to retard the of the brain that occurs during Alzheimer's disease. Chapters cover continuous degeneration topics from growth factor secretion of proteases, which could modify amyloid processing, to neuronal gene delivery using viral vectors. The breadth and thoroughness of the chapters truly embrace a broad spectrurn of models, pathological mechanisms and therapeutic approaches
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