Strategies for disease modification in Alzheimer's disease

[1]  Z. Stelmasiak,et al.  [Highlights from the American Academy of Neurology's 56th Annual Meeting 24 April-1 May 2004, San Francisco, USA]. , 2004, Neurologia i neurochirurgia polska.

[2]  Jay S. Fine,et al.  Chronic Treatment with the γ-Secretase Inhibitor LY-411,575 Inhibits β-Amyloid Peptide Production and Alters Lymphopoiesis and Intestinal Cell Differentiation* , 2004, Journal of Biological Chemistry.

[3]  M. Citron.  Beta-secretase inhibition for the treatment of Alzheimer's disease--promise and challenge. , 2004, Trends in pharmacological sciences.

[4]  C. Fowler.  Possible involvement of the endocannabinoid system in the actions of three clinically used drugs. , 2004, Trends in pharmacological sciences.

[5]  B. Wolozin,et al.  Cholesterol and the Biology of Alzheimer's Disease , 2004, Neuron.

[6]  M. Ohno,et al.  BACE1 Deficiency Rescues Memory Deficits and Cholinergic Dysfunction in a Mouse Model of Alzheimer's Disease , 2004, Neuron.

[7]  I. Ferrer,et al.  Neuropathology and Pathogenesis of Encephalitis following Amyloid β Immunization in Alzheimer's Disease , 2004, Brain pathology.

[8]  B. de Strooper,et al.  The Cell Adhesion Protein P-selectin Glycoprotein Ligand-1 Is a Substrate for the Aspartyl Protease BACE1* , 2003, Journal of Biological Chemistry.

[9]  S. Ferris.  Evaluation of memantine for the treatment of Alzheimer’s disease , 2003, Expert opinion on pharmacotherapy.

[10]  A. Mackinnon,et al.  Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial. , 2003, Archives of neurology.

[11]  M. Pangalos,et al.  BACE1 (β-secretase) transgenic and knockout mice: identification of neurochemical deficits and behavioral changes , 2003, Molecular and Cellular Neuroscience.

[12]  M. Citron,et al.  BACE1 (β-secretase) knockout mice do not acquire compensatory gene expression changes or develop neural lesions over time , 2003, Neurobiology of Disease.

[13]  R. Heinrikson,et al.  Human β-Secretase (BACE) and BACE Inhibitors , 2003 .

[14]  P. Adamson,et al.  How do statins control neuroinflammation? , 2003, Inflammation Research.

[15]  S. Weggen,et al.  Evidence That Nonsteroidal Anti-inflammatory Drugs Decrease Amyloid β42 Production by Direct Modulation of γ-Secretase Activity* , 2003, Journal of Biological Chemistry.

[16]  S. Weggen,et al.  The Non-cyclooxygenase Targets of Non-steroidal Anti-inflammatory Drugs, Lipoxygenases, Peroxisome Proliferator-activated Receptor, Inhibitor of κB Kinase, and NFκB, Do Not Reduce Amyloid β42 Production* , 2003, Journal of Biological Chemistry.

[17]  M. Citron,et al.  Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease , 2003, The Journal of Neuroscience.

[18]  C. Finch,et al.  Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[19]  B. Dubois,et al.  Subacute meningoencephalitis in a subset of patients with AD after Aβ42 immunization , 2003, Neurology.

[20]  K. Davis,et al.  Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. , 2003, JAMA.

[21]  S. Yamazaki,et al.  The γ-Secretase Inhibitor N-[N-(3,5-Difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl Ester Reduces Aβ Levels in Vivo in Plasma and Cerebrospinal Fluid in Young (Plaque-Free) and Aged (Plaque-Bearing) Tg2576 Mice , 2003, Journal of Pharmacology and Experimental Therapeutics.

[22]  K. Henke,et al.  Antibodies against β-Amyloid Slow Cognitive Decline in Alzheimer's Disease , 2003, Neuron.

[23]  Kazuyuki Takata,et al.  Cdk5 Is a Key Factor in Tau Aggregation and Tangle Formation In Vivo , 2003, Neuron.

[24]  J. Regula,et al.  Reconstitution of γ-secretase activity , 2003, Nature Cell Biology.

[25]  S. Kitazume,et al.  Characterization of α2,6-Sialyltransferase Cleavage by Alzheimer's β-Secretase (BACE1)* , 2003, The Journal of Biological Chemistry.

[26]  B. Strooper,et al.  Aph-1, Pen-2, and Nicastrin with Presenilin Generate an Active γ-Secretase Complex , 2003, Neuron.

[27]  D. Brooks,et al.  Direct brain infusion of glial cell line–derived neurotrophic factor in Parkinson disease , 2003, Nature Medicine.

[28]  C. Holmes,et al.  Neuropathology of human Alzheimer disease after immunization with amyloid-β peptide: a case report , 2003, Nature Medicine.

[29]  R. Motter,et al.  Epitope and isotype specificities of antibodies to β-amyloid peptide for protection against Alzheimer's disease-like neuropathology , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[30]  W. Oertel,et al.  Treatment with the selective muscarinic ml agonist talsaclidine decreases cerebrospinal fluid levels of Aβ42 in patients with Alzheimer's disease , 2003, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.

[31]  M. Staufenbiel,et al.  Cerebral Hemorrhage After Passive Anti-Aβ Immunotherapy , 2002, Science.

[32]  B. Hyman,et al.  Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. , 2002, Archives of neurology.

[33]  C. Masters,et al.  Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease , 2002 .

[34]  Xin Wu,et al.  Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model , 2002, Nature Neuroscience.

[35]  C. Goetz.  Special Issue: Selected Essays From the American Academy of Neurology Educational Program, 2001 , 2002 .

[36]  W. K. Cullen,et al.  Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.

[37]  Rong Wang,et al.  A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity , 2001, Nature.

[38]  S. Kitazume,et al.  Alzheimer's β-secretase, β-site amyloid precursor protein-cleaving enzyme, is responsible for cleavage secretion of a Golgi-resident sialyltransferase , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[39]  Patrick L. McGeer,et al.  Inflammation, autotoxicity and Alzheimer disease , 2001, Neurobiology of Aging.

[40]  B. Hyman,et al.  Acyl-coenzyme A: cholesterol acyltransferase modulates the generation of the amyloid β-peptide , 2001, Nature Cell Biology.

[41]  Lin Hong,et al.  Subsite Specificity of Memapsin 2 (β-Secretase): Implications for Inhibitor Design† , 2001 .

[42]  K. Duff,et al.  Permeability of Proteins at the Blood–Brain Barrier in the Normal Adult Mouse and Double Transgenic Mouse Model of Alzheimer's Disease , 2001, Neurobiology of Disease.

[43]  R. Perlmutter,et al.  Presenilin-dependent γ-secretase activity modulates thymocyte development , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[44]  David J. Cummins,et al.  Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[45]  Gregory D. Longmore,et al.  γ-Secretase inhibitors repress thymocyte development , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[46]  I. Kola,et al.  BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics. , 2001, Human molecular genetics.

[47]  C. Masters,et al.  Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice , 2001, Neuron.

[48]  M. Staufenbiel,et al.  Spontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy , 2001, The Journal of Neuroscience.

[49]  H. Cai,et al.  BACE1 is the major β-secretase for generation of Aβ peptides by neurons , 2001, Nature Neuroscience.

[50]  C. Schweiger.  [Statins and the risk of dementia]. , 2001, Italian heart journal. Supplement : official journal of the Italian Federation of Cardiology.

[51]  W. Richards,et al.  Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.

[52]  J. Hardy,et al.  Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease , 2000, Nature.

[53]  Ralph A. Nixon,et al.  Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease , 2000, Nature.

[54]  B. Solomon,et al.  Immunization against Alzheimer's beta -amyloid plaques via EFRH phage administration. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[55]  L Hong,et al.  Structure of the protease domain of memapsin 2 (beta-secretase) complexed with inhibitor. , 2000, Science.

[56]  M. Schell,et al.  Antibody-mediated resolution of light chain-associated amyloid deposits. , 2000, The American journal of pathology.

[57]  G. Celesia,et al.  Decreased prevalence of Alzheimer disease associated with 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitors. , 2000, Archives of neurology.

[58]  K. Ashe,et al.  Ibuprofen Suppresses Plaque Pathology and Inflammation in a Mouse Model for Alzheimer's Disease , 2000, The Journal of Neuroscience.

[59]  R. Motter,et al.  Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease , 2000, Nature Medicine.

[60]  Wen-Lang Lin,et al.  Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein , 2000, Nature Genetics.

[61]  A. Fisher.  M1 muscarinic agonists: Their potential in treatment and as disease‐modifying agents in Alzheimer's disease , 2000 .

[62]  F. D. Miller,et al.  Functional gamma‐secretase inhibitors reduce beta‐amyloid peptide levels in brain , 2000, Journal of neurochemistry.

[63]  J. Drews.  Drug discovery: a historical perspective. , 2000, Science.

[64]  R. Barbour,et al.  Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.

[65]  Alfredo G. Tomasselli,et al.  Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.

[66]  David G. Tew,et al.  Identification of a Novel Aspartic Protease (Asp 2) as β-Secretase , 1999, Molecular and Cellular Neuroscience.

[67]  Rudolph E. Tanzi,et al.  BACE Maps to Chromosome 11 and a BACE Homolog, BACE2, Reside in the Obligate Down Syndrome Region of Chromosome 21 , 1999 .

[68]  R. Doody.  Therapeutic standards in Alzheimer disease. , 1999, Alzheimer disease and associated disorders.

[69]  John Q Trojanowski,et al.  Neurodegenerative Tauopathies Human Disease and Transgenic Mouse Models , 1999, Neuron.

[70]  J. Treanor,et al.  Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.

[71]  R. Motter,et al.  Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse , 1999, Nature.

[72]  D. Selkoe,et al.  Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity , 1999, Nature.

[73]  William J. Ray,et al.  A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain , 1999, Nature.

[74]  H. Möller.  Reappraising neurotransmitter-based strategies , 1999, European Neuropsychopharmacology.

[75]  B. Winblad,et al.  Intracerebroventricular Infusion of Nerve Growth Factor in Three Patients with Alzheimer’s Disease , 1998, Dementia and Geriatric Cognitive Disorders.

[76]  S. Enna,et al.  Pharmacological Management of Neurological and Psychiatric Disorders , 1998 .

[77]  B. Sommer,et al.  Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[78]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[79]  Patrick L. McGeer,et al.  Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease , 1996, Neurology.

[80]  J. Haines,et al.  Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. , 1993, Science.

[81]  A. Kaszniak,et al.  Clinical trial of indomethacin in Alzheimer's disease , 1993, Neurology.

[82]  P. Lansbury,et al.  The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation: implications for the pathogenesis of Alzheimer's disease. , 1993, Biochemistry.

[83]  P. Greengard,et al.  Cholinergic agonists and interleukin 1 regulate processing and secretion of the Alzheimer beta/A4 amyloid protein precursor. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[84]  J. Growdon,et al.  Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors. , 1992, Science.

[85]  S. Estus,et al.  Production of the Alzheimer amyloid beta protein by normal proteolytic processing. , 1992, Science.

[86]  D. Selkoe,et al.  Amyloid β-peptide is produced by cultured cells during normal metabolism , 1992, Nature.

[87]  Bradley T. Hyman,et al.  Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.

[88]  C. Sing,et al.  Role of the apolipoprotein E polymorphism in determining normal plasma lipid and lipoprotein variation. , 1985, American journal of human genetics.

[89]  D. Werring,et al.  Randomized Controlled Trial , 2020, Encyclopedia of Behavioral Medicine.

[90]  Rena Li,et al.  Amyloid (cid:1) peptide load is correlated with increased (cid:1) -secretase activity in sporadic Alzheimer’s disease patients , 2004 .

[91]  A. Sands,et al.  Knockouts model the 100 best-selling drugs—will they model the next 100? , 2003, Nature Reviews Drug Discovery.

[92]  P. Wong,et al.  Elevated β-secretase expression and enzymatic activity detected in sporadic Alzheimer disease , 2003, Nature Medicine.

[93]  A. Mackinnon,et al.  Metal-Protein Attenuation With Iodochlorhydroxyquin (Clioquinol) Targeting A Amyloid Deposition and Toxicity in Alzheimer Disease , 2003 .

[94]  D. Fairlie,et al.  Protease inhibitors: current status and future prospects. , 2000, Journal of medicinal chemistry.

[95]  Jeremy Fairbank,et al.  Historical Perspective , 1987, Do We Really Understand Quantum Mechanics?.

[96]  D. C. Henckel,et al.  Case report. , 1995, Journal.

[97]  J. Hardy,et al.  Amyloid deposition as the central event in the aetiology of Alzheimer's disease. , 1991, Trends in pharmacological sciences.