Works matching IS 00778923 AND DT 2000 AND VI 920 AND IP 1
Results: 48
Treatment with the Selective Muscarinic Agonist Talsaclidine Decreases Cerebrospinal Fluid Levels of Total Amyloid β-Peptide in Patients with Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 285, doi. 10.1111/j.1749-6632.2000.tb06937.x
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Activated Mitogenic Signaling Induces a Process of Dedifferentiation in Alzheimer's Disease That Eventually Results in Cell Death.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 249, doi. 10.1111/j.1749-6632.2000.tb06931.x
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Presenilin-1: A Component of Synaptic and Endothelial Adherens Junctions.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 209, doi. 10.1111/j.1749-6632.2000.tb06924.x
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Modulation of Aβ Deposition in APP Transgenic Mice by an Apolipoprotein E Null Background.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 171, doi. 10.1111/j.1749-6632.2000.tb06919.x
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Cholinesterase Inhibitors Stabilize Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 321, doi. 10.1111/j.1749-6632.2000.tb06942.x
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The Clinical Spectrum of Guam ALS and Parkinson-Dementia Complex: 1997-1999.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 120, doi. 10.1111/j.1749-6632.2000.tb06913.x
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Prevention and Reduction of AD-type Pathology in PDAPP Mice Immunized with Aβ<sub>1-42</sub>.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 274, doi. 10.1111/j.1749-6632.2000.tb06936.x
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α1-Antichymotrypsin Inhibits Aβ Degradation in Vitro and in Vivo.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 245, doi. 10.1111/j.1749-6632.2000.tb06930.x
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The Value of Transgenic Models for the Study of Neurodegenerative Diseases.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 179, doi. 10.1111/j.1749-6632.2000.tb06920.x
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Inhibition of the Neuronal Insulin Receptor An in Vivo Model for Sporadic Alzheimer Disease?
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 256, doi. 10.1111/j.1749-6632.2000.tb06932.x
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Progress in Hereditary Tauopathies: A Mutation in the Tau Gene (G389R) Causes a Pick Disease-like Syndrome.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 52, doi. 10.1111/j.1749-6632.2000.tb06905.x
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GSK3β Forms a Tetrameric Complex with Endogenous PS1-CTF/NTF and β-Catenin: Effects of the D257/D385A and FAD-linked Mutations.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 227, doi. 10.1111/j.1749-6632.2000.tb06927.x
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Molecular Genetics of Chromosome 17 Tauopathies.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 63, doi. 10.1111/j.1749-6632.2000.tb06906.x
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Tau Gene Mutations in Frontotemporal Dementia and Parkinsonism Linked to Chromosome 17 (FTDP-17): Their Relevance for Understanding the Neurogenerative Process.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 74, doi. 10.1111/j.1749-6632.2000.tb06907.x
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Toward the Characterization and Identification of γ-Secretases Using Transition-state Analogue Inhibitors.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 197, doi. 10.1111/j.1749-6632.2000.tb06922.x
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Cytidine (5′) Diphosphocholine Modulates Dopamine K<sup>+</sup>-evoked Release in Striatum Measured by Microdialysis.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 332, doi. 10.1111/j.1749-6632.2000.tb06944.x
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The α-Synucleinopathies: Parkinson's Disease, Dementia with Lewy Bodies, and Multiple System Atrophy.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 16, doi. 10.1111/j.1749-6632.2000.tb06900.x
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An Empirical Model of γ-Secretase Activity.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 233, doi. 10.1111/j.1749-6632.2000.tb06928.x
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Cytoplasmic Presenilin Aggregates in Proteasome Inhibitor-treated Cells.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 259, doi. 10.1111/j.1749-6632.2000.tb06933.x
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Nasal Aβ Treatment Induces Anti-Aβ Antibody Production and Decreases Cerebral Amyloid Burden in PD-APP Mice.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 328, doi. 10.1111/j.1749-6632.2000.tb06943.x
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Coexistent Tau and Amyloid Pathology in Hereditary Frontotemporal Dementia with Tau Mutations.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 115, doi. 10.1111/j.1749-6632.2000.tb06912.x
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Rapid Notch1 Nuclear Translocation after Ligand Binding Depends on Presenilin-associated γ-Secretase Activity.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 223, doi. 10.1111/j.1749-6632.2000.tb06926.x
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Clinical Lewy Body Syndromes.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 1, doi. 10.1111/j.1749-6632.2000.tb06898.x
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α-Secretase Activity of the Disintegrin Metalloprotease ADAM 10: Influences of Domain Structure.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 215, doi. 10.1111/j.1749-6632.2000.tb06925.x
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Identifying Proteases That Cleave APP.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 192, doi. 10.1111/j.1749-6632.2000.tb06921.x
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Pathogenic Mechanisms of Alzheimer's Disease Analyzed in the APP23 Transgenic Mouse Model.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 134, doi. 10.1111/j.1749-6632.2000.tb06915.x
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Clinical and Neuropathological Correlates of Dementia with Lewy Bodies.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 9, doi. 10.1111/j.1749-6632.2000.tb06899.x
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Physiology and Pathophysiology of α-Synuclein: Cell Culture and Transgenic Animal Models Based on a Parkinson's Disease-associated Protein.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 33, doi. 10.1111/j.1749-6632.2000.tb06902.x
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Amyloidogenesis in Familial British Dementia Is Associated with a Genetic Defect on Chromosome 13.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 84, doi. 10.1111/j.1749-6632.2000.tb06908.x
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Regulation of APP Synthesis and Secretion by Neuroimmunophilin Ligands and Cyclooxygenase Inhibitors.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 261, doi. 10.1111/j.1749-6632.2000.tb06934.x
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High Frequency of Mutations in Four Different Disease Genes in Early-Onset Dementia.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 100, doi. 10.1111/j.1749-6632.2000.tb06910.x
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Prions: Pathogenesis and Reverse Genetics.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 140, doi. 10.1111/j.1749-6632.2000.tb06916.x
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Aβ Modulation: The Next Generation of AD Therapeutics.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 269, doi. 10.1111/j.1749-6632.2000.tb06935.x
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Cholinergic Modulation of Amyloid Processing and Dementia in Animal Models of Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 309, doi. 10.1111/j.1749-6632.2000.tb06940.x
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Pathological Tau Phenotypes: The Weight of Mutations, Polymorphisms, and Differential Neuronal Vulnerabilities.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 107, doi. 10.1111/j.1749-6632.2000.tb06911.x
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In Vivo Analysis of Wild-type and FTDP-17 Tau Transgenic Mice.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 126, doi. 10.1111/j.1749-6632.2000.tb06914.x
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Preface.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. xi, doi. 10.1111/j.1749-6632.2000.tb06897.x
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Regulation of Gene Expression by Muscarinic Acetylcholine Receptors: A Comprehensive Approach for the Identification of Regulated Genes.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 305, doi. 10.1111/j.1749-6632.2000.tb06939.x
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Recent Advances in the Understanding of the Processing of APP to Beta Amyloid Peptide.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 206, doi. 10.1111/j.1749-6632.2000.tb06923.x
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Role of Presenilin-1 in Murine Neural Development.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 165, doi. 10.1111/j.1749-6632.2000.tb06918.x
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Presenilin Function in APP Processing.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 158, doi. 10.1111/j.1749-6632.2000.tb06917.x
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Accelerated Oligomerization by Parkinson's Disease Linked α-Synuclein Mutants.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 42, doi. 10.1111/j.1749-6632.2000.tb06903.x
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Familial British Dementia: Expression and Metabolism of BRI.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 93, doi. 10.1111/j.1749-6632.2000.tb06909.x
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Classification and Description of Frontotemporal Dementias.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 46, doi. 10.1111/j.1749-6632.2000.tb06904.x
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Genetics of Parkinson's Disease.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 28, doi. 10.1111/j.1749-6632.2000.tb06901.x
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M1 Muscarinic Agonists as Potential Disease-Modifying Agents in Alzheimer's Disease: Rationale and Perspectives.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 315, doi. 10.1111/j.1749-6632.2000.tb06941.x
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Overexpression of Presenilin-2 Enhances Apoptotic Death of Cultured Cortical Neurons.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 241, doi. 10.1111/j.1749-6632.2000.tb06929.x
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Metal Chelation as a Potential Therapy for Alzheimer's Disease.
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- Annals of the New York Academy of Sciences, 2000, v. 920, n. 1, p. 292, doi. 10.1111/j.1749-6632.2000.tb06938.x
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