Works matching IS 00778923 AND DT 1993 AND VI 695 AND IP 1
Results: 63
Comparative Effects of Aging Process on Phosphatidylcholine Biosynthesis Pathway: A Key Role for CTP-Phosphocholine Cytidylyltransferase?
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 86, doi. 10.1111/j.1749-6632.1993.tb23034.x
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Receptor-coupled Amyloid Precursor Protein Processing.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 122, doi. 10.1111/j.1749-6632.1993.tb23039.x
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The C-Terminus of the β Protein is Critical in Amyloidogenesis.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 144, doi. 10.1111/j.1749-6632.1993.tb23043.x
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The Amyloid Precursor Protein in Ischemic Brain Injury and Chronic Hypoperfusion.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 190, doi. 10.1111/j.1749-6632.1993.tb23050.x
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Cholinergic and Non-cholinergic Synaptic Mechanisms in the Aged Rat Hippocampus.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 236, doi. 10.1111/j.1749-6632.1993.tb23059.x
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Protein Phosphorylation Regulates Relative Utilization of Processing Pathways for Alzheimer β/A4 Amyloid Precursor Protein.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 117, doi. 10.1111/j.1749-6632.1993.tb23038.x
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Regulation of Amyloid Precursor Protein Release By Protein Kinase C in Swiss 3T3 Fibroblasts.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 128, doi. 10.1111/j.1749-6632.1993.tb23040.x
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Sequestration of Amyloid β-Peptide.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 139, doi. 10.1111/j.1749-6632.1993.tb23042.x
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Effect of CDP-Choline on Cognition and Immune Function in Alzheimer's Disease and Multi-Infarct Dementia.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 321, doi. 10.1111/j.1749-6632.1993.tb23076.x
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The Use of the Computerized Neuropsychological Test Battery (CNTB) in an Efficacy and Safety Trial of BMY 21,502 in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 332, doi. 10.1111/j.1749-6632.1993.tb23079.x
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Second Messengers in Neuronal Signaling.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 10, doi. 10.1111/j.1749-6632.1993.tb23019.x
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NMDA Receptor Status in Elderly Normal Individuals and Those with Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 50, doi. 10.1111/j.1749-6632.1993.tb23026.x
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Gangliosides and Neurotrophic Factors in Neurodegenerative Diseases: From Experimental Findings to Clinical Perspectives.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 314, doi. 10.1111/j.1749-6632.1993.tb23074.x
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PKC Translocation in Rat Brain Cortex Is Promoted in Vivo and in Vitro by α-Glycerylphosphorylcholine, a Cognition-enhancing Drug.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 307, doi. 10.1111/j.1749-6632.1993.tb23072.x
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X-Ray Diffraction Analysis of Brain Lipid Membrane Structure in Alzheimer's Disease and β-Amyloid Peptide Interactions.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 54, doi. 10.1111/j.1749-6632.1993.tb23027.x
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Oral Cytidine 5′-Diphosphate Choline Administration to Rats Increases Brain Phospholipid Levels.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 318, doi. 10.1111/j.1749-6632.1993.tb23075.x
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Protease Inhibitors and Indolamines Selectively Inhibit Cholinesterases in the Histopathologic Structures of Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 65, doi. 10.1111/j.1749-6632.1993.tb23029.x
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Decreased Density of Forebrain Cholinergic Neurons and Disintegration of the Spatial Organization of Behavior in Experimental Autoimmune Dementia (EAD).
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 244, doi. 10.1111/j.1749-6632.1993.tb23061.x
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Principles of Synaptic Transmission.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 1, doi. 10.1111/j.1749-6632.1993.tb23018.x
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Transmitters in the Developing and Senescent Human Brain.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 69, doi. 10.1111/j.1749-6632.1993.tb23030.x
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Normal Cellular Processing of the β-Amyloid Precursor Protein Results in the Secretion of the Amyloid β Peptide and Related Molecules.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 109, doi. 10.1111/j.1749-6632.1993.tb23037.x
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Biologically Active Domain of the Secreted Form of the Amyloid β/A4 Protein Precursor.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 149, doi. 10.1111/j.1749-6632.1993.tb23044.x
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Preface.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. xiii, doi. 10.1111/j.1749-6632.1993.tb23017.x
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Acetyl-.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 324, doi. 10.1111/j.1749-6632.1993.tb23077.x
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Changes in G Protein-mediated Signal Transduction in Aging and Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 42, doi. 10.1111/j.1749-6632.1993.tb23024.x
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The Age of Biosenescence and the Incidence of Cerebral β-Amyloidosis in Aged Captive Rhesus Monkeys.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 232, doi. 10.1111/j.1749-6632.1993.tb23058.x
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Search for the Genes Responsible for Familial Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 203, doi. 10.1111/j.1749-6632.1993.tb23053.x
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Age-related Cognitive Deficits in Rats Are Associated with a Combined Loss of Cholinergic and Serotonergic Functions.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 254, doi. 10.1111/j.1749-6632.1993.tb23063.x
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Aberrant Phosphoinositide Metabolism in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 46, doi. 10.1111/j.1749-6632.1993.tb23025.x
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Dopamine D2 Receptors in Normal Human Brain: Effect of Age Measured by Positron Emission Tomography (PET) and [.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 81, doi. 10.1111/j.1749-6632.1993.tb23033.x
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Hyperactivation of Signal Transduction Systems in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 34, doi. 10.1111/j.1749-6632.1993.tb23023.x
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Production of Amyloid β Protein from Normal Amyloid β-Protein Precursor (βAPP) and the Mutated βAPPS Linked to Familial Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 103, doi. 10.1111/j.1749-6632.1993.tb23036.x
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Transgenic Mice Expressing Human β-APP751, But Not Mice Expressing β-APP695, Display Early Alzheimer's Disease-like Histopathology.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 224, doi. 10.1111/j.1749-6632.1993.tb23056.x
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Neural Transplantation for Neurodegenerative Diseases: Past, Present, and Future.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 258, doi. 10.1111/j.1749-6632.1993.tb23064.x
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In Vivo Detection of Neurotransmitter Changes in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 27, doi. 10.1111/j.1749-6632.1993.tb23022.x
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Cellular Processing and Proteoglycan Nature of Amyloid Precursor Proteins.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 132, doi. 10.1111/j.1749-6632.1993.tb23041.x
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Activation PET as an Instrument to Determine Therapeutic Efficacy in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 327, doi. 10.1111/j.1749-6632.1993.tb23078.x
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Transgenic Animal Models for Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 217, doi. 10.1111/j.1749-6632.1993.tb23055.x
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Expression of L-APP mRNA in Brain Cells.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 183, doi. 10.1111/j.1749-6632.1993.tb23049.x
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Experimental Induction of β-Amyloid Plaques and Cerebral Angiopathy in Primates.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 228, doi. 10.1111/j.1749-6632.1993.tb23057.x
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Heat-shocked Neuronal PC12 Cells Reveal Alzheimer's Disease-associated Alterations in Amyloid Precursor Protein and Tau.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 194, doi. 10.1111/j.1749-6632.1993.tb23051.x
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A New Hypothesis for the Mechanism of Amyloid Toxicity, Based on the Calcium Channel Activity of Amyloid β Protein (AβP) in Phospholipid Bilayer Membranes.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 165, doi. 10.1111/j.1749-6632.1993.tb23046.x
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Natural and Synthetic Huperzine A: Effect on Cholinergic Function in Vitro and in Vivo.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 304, doi. 10.1111/j.1749-6632.1993.tb23071.x
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Alzheimer's Disease Families with Amyloid Precursor Protein Mutations.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 198, doi. 10.1111/j.1749-6632.1993.tb23052.x
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The Role of Extracellular Matrix in the Processing of the Amyloid Protein Precursor of Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 169, doi. 10.1111/j.1749-6632.1993.tb23047.x
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Abnormalities in Brain Glucose Utilization and Its Impact on Cellular and Molecular Mechanisms in Sporadic Dementia of Alzheimer Type.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 77, doi. 10.1111/j.1749-6632.1993.tb23032.x
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Cholinergic Neurotransmission in the Hippocampus of Aged Rats: Influence of L-α-Glycerylphosphorylcholine Treatment.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 311, doi. 10.1111/j.1749-6632.1993.tb23073.x
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β-Amyloid Precursor Protein Mismetabolism and Loss of Calcium Homeostasis in Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 158, doi. 10.1111/j.1749-6632.1993.tb23045.x
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Regulation and Expression of the Alzheimer's β/A4 Amyloid Protein Precursor in Health, Disease, and Down's Syndrome.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 91, doi. 10.1111/j.1749-6632.1993.tb23035.x
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Phospholipid and Phospholipid Metabolites in Rat Frontal Cortex Are Decreased following Nucleus Basalis Lesions.
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- Annals of the New York Academy of Sciences, 1993, v. 695, n. 1, p. 241, doi. 10.1111/j.1749-6632.1993.tb23060.x
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