Wnt signaling function in Alzheimer’s disease

[1]  M. Mesulam,et al.  Cholinesterases within neurofibrillary tangles related to age and Alzheimer's disease , 1987, Annals of neurology.

[2]  C. Geula,et al.  Acetylcholinesterase‐rich pyramidal neurons in the human neocortex and hippocampus: Absence at birth, development during the life span, and dissolution in Alzheimer's disease , 1988, Annals of neurology.

[3]  K. Dobkins,et al.  Decreased levels of protein kinase C in Alzheimer brain , 1988, Brain Research.

[4]  C. Geula,et al.  Special properties of cholinesterases in the cerebral cortex of Alzheimer's disease , 1989, Brain Research.

[5]  R. Katzman.,et al.  Reduced protein kinase C immunoreactivity and altered protein phosphorylation in Alzheimer's disease fibroblasts. , 1989, Archives of neurology.

[6]  D. Kirschner,et al.  Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.

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

[8]  J. Hardy,et al.  Alzheimer's disease: the amyloid cascade hypothesis. , 1992, Science.

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

[10]  Bradley T. Hyman,et al.  Distribution of Alzheimer‐type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease , 1992, Neurology.

[11]  A. Takashima.  Tau protein I is essential for amyloid β-protein iduced neurotoxicity , 1993 .

[12]  J. Growdon,et al.  Activation of protein kinase C inhibits cellular production of the amyloid beta-protein. , 1993, The Journal of biological chemistry.

[13]  M. Hagiwara,et al.  Assessment of protein kinase C isozymes by two‐site enzyme immunoassay in human brains and changes in Alzheimer's disease , 1993, Neurology.

[14]  K. Imahori,et al.  Tau protein kinase I is essential for amyloid beta-protein-induced neurotoxicity. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[15]  B. Hyman,et al.  The Lack of Accumulation of Senile Plaques or Amyloid Burden in Alzheimer's Disease Suggests a Dynamic Balance Between Amyloid Deposition and Resolution , 1993, Journal of neuropathology and experimental neurology.

[16]  A. McMahon,et al.  Mouse Wnt genes exhibit discrete domains of expression in the early embryonic CNS and limb buds. , 1993, Development.

[17]  G. Binetti,et al.  Cytosol protein kinase C downregulation in fibroblasts from Alzheimer's disease patients , 1993, Neurology.

[18]  B. Yankner,et al.  Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[19]  Claudia H. Kawas,et al.  The epidemiology of dementia and Alzheimer disease. , 1994 .

[20]  H. Theisen,et al.  dishevelled is required during wingless signaling to establish both cell polarity and cell identity. , 1994, Development.

[21]  C. Soto,et al.  Structural Determinants of the Alzheimer's Amyloid β‐Peptide , 1994 .

[22]  N. Perrimon,et al.  Isolation and characterization of a mouse homolog of the Drosophila segment polarity gene dishevelled. , 1994, Developmental biology.

[23]  A. McMahon,et al.  Wnt genes and vertebrate development. , 1994, Current opinion in genetics & development.

[24]  S. Pelech.  Networking with proline-directed protein kinases implicated in Tau phosphorylation , 1995, Neurobiology of Aging.

[25]  S. Blair,et al.  Notch regulates wingless expression and is not required for reception of the paracrine wingless signal during wing margin neurogenesis in Drosophila. , 1995, Development.

[26]  R. Moon,et al.  Zebrafish wnt8 and wnt8b share a common activity but are involved in distinct developmental pathways. , 1995, Development.

[27]  S. Lovestone,et al.  Modulation of PHF-like tau phosphorylation in cultured neurones and transfected cells , 1995, Neurobiology of Aging.

[28]  H. Braak,et al.  Staging of alzheimer's disease-related neurofibrillary changes , 1995, Neurobiology of Aging.

[29]  K. Imahori,et al.  Amyloid β peptide induces cytoplasmic accumulation of amyloid protein precursor via tau protein kinase I/glycogen synthase kinase-3β in rat hippocampal neurons , 1995, Neuroscience Letters.

[30]  C. Soto,et al.  The -Helical to -Strand Transition in the Amino-terminal Fragment of the Amyloid -Peptide Modulates Amyloid Formation * , 1995, The Journal of Biological Chemistry.

[31]  H. Jäckle,et al.  Invagination centers within the Drosophila stomatogastric nervous system anlage are positioned by Notch-mediated signaling which is spatially controlled through wingless. , 1995, Development.

[32]  H. Manji,et al.  Signal transduction pathways. Molecular targets for lithium's actions. , 1995, Archives of general psychiatry.

[33]  B. Yankner,et al.  β-Amyloid fibrils induce tau phosphorylation and loss of microtubule binding , 1995, Neuron.

[34]  D. Price,et al.  Expression of Presenilin 1 and 2 (PS1 and PS2) in Human and Murine Tissues , 1996, The Journal of Neuroscience.

[35]  N. Perrimon,et al.  Conservation of dishevelled structure and function between flies and mice: isolation and characterization of Dvl2 , 1996, Mechanisms of Development.

[36]  D. Selkoe,et al.  Amyloid β-Protein and the Genetics of Alzheimer's Disease* , 1996, The Journal of Biological Chemistry.

[37]  N. Perrimon,et al.  Interaction Between Wingless and Notch Signaling Pathways Mediated by Dishevelled , 1996, Science.

[38]  C. Soto,et al.  Extracellular matrix regulates the amount of the β‐amyloid precursor protein and its amyloidogenic fragments , 1996, Journal of cellular physiology.

[39]  James R. Woodgett,et al.  Lithium inhibits glycogen synthase kinase-3 activity and mimics Wingless signalling in intact cells , 1996, Current Biology.

[40]  C. Ponting,et al.  Pleckstrin's repeat performance: a novel domain in G-protein signaling? , 1996, Trends in biochemical sciences.

[41]  K. Imahori,et al.  Exposure of rat hippocampal neurons to amyloid β peptide (25–35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3β , 1996, Neuroscience Letters.

[42]  R. Cowburn,et al.  Neurotransmitters, signal transduction and second‐messengers in Alzheimer's disease , 1996, Acta neurologica Scandinavica. Supplementum.

[43]  N. Inestrosa,et al.  Amyloid precursor protein fragment and acetylcholinesterase increase with cell confluence and differentiation in a neuronal cell line. , 1996, Experimental cell research.

[44]  D. Melton,et al.  A molecular mechanism for the effect of lithium on development. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[45]  Brian J Cummings,et al.  β-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease , 1996, Neurobiology of Aging.

[46]  B. Hyman,et al.  Alzheimer–associated presenilins 1 and 2 : Neuronal expression in brain and localization to intracellular membranes in mammalian cells , 1996, Nature Medicine.

[47]  R. Moon,et al.  The axis-inducing activity, stability, and subcellular distribution of beta-catenin is regulated in Xenopus embryos by glycogen synthase kinase 3. , 1996, Genes & development.

[48]  N. Inestrosa,et al.  Laminin inhibits amyloid-β-peptide fibrillation , 1996, Neuroscience Letters.

[49]  J. Woodgett,et al.  Wingless inactivates glycogen synthase kinase‐3 via an intracellular signalling pathway which involves a protein kinase C. , 1996, The EMBO journal.

[50]  G. Schellenberg,et al.  Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.

[51]  D. Beier,et al.  Isolation and characterization of mouse Dishevelled‐3 , 1996, Developmental dynamics : an official publication of the American Association of Anatomists.

[52]  Claudia Linker,et al.  Acetylcholinesterase Accelerates Assembly of Amyloid-β-Peptides into Alzheimer's Fibrils: Possible Role of the Peripheral Site of the Enzyme , 1996, Neuron.

[53]  K. Beyreuther,et al.  Formation of stable complexes between two Alzheimer's disease gene products: Presenilin-2 and β-amyloid precursor protein , 1997, Nature Medicine.

[54]  D. Selkoe,et al.  Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[55]  Khadija Iqbal,et al.  Abnormal phosphorylation of tau and the mechanism of Alzheimer neurofibrillary degeneration: sequestration of microtubule-associated proteins 1 and 2 and the disassembly of microtubules by the abnormal tau. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[56]  M. Lovett,et al.  Presenilin 1 interaction in the brain with a novel member of the Armadillo family , 1997, Neuroreport.

[57]  M. Semënov,et al.  Human dishevelled genes constitute a DHR-containing multigene family. , 1997, Genomics.

[58]  B. Anderton,et al.  Stress‐Activated Protein Kinase/c‐Jun N‐Terminal Kinase Phosphorylates τ Protein , 1997, Journal of neurochemistry.

[59]  E. Braak,et al.  Distribution, Levels, and Activity of Glycogen Synthase Kinase‐3 in the Alzheimer Disease Brain , 1997, Journal of neuropathology and experimental neurology.

[60]  D. Borchelt,et al.  Endoproteolytic Processing and Stabilization of Wild-type and Mutant Presenilin* , 1997, The Journal of Biological Chemistry.

[61]  J. Ávila,et al.  Lithium inhibits Alzheimer's disease‐like tau protein phosphorylation in neurons , 1997, FEBS letters.

[62]  C. L. Harris,et al.  Evidence That Levels of Presenilins (PS1 and PS2) Are Coordinately Regulated by Competition for Limiting Cellular Factors* , 1997, The Journal of Biological Chemistry.

[63]  Richard Paylor,et al.  Social Interaction and Sensorimotor Gating Abnormalities in Mice Lacking Dvl1 , 1997, Cell.

[64]  I. Kanazawa,et al.  Presenilin 1 binds to amyloid precursor protein directly. , 1997, Biochemical and biophysical research communications.

[65]  R. Faull,et al.  Expression of Fos, Jun, and Krox Family Proteins in Alzheimer's Disease , 1997, Experimental Neurology.

[66]  C. Haass.  Presenilins: Genes for Life and Death , 1997, Neuron.

[67]  R. Moon,et al.  Interaction of Wnt and a Frizzled homologue triggers G-protein-linked phosphatidylinositol signalling , 1997, Nature.

[68]  Jörg Stappert,et al.  β‐catenin is a target for the ubiquitin–proteasome pathway , 1997 .

[69]  Y. Kitamura,et al.  Changes of p53 in the brains of patients with Alzheimer's disease. , 1997, Biochemical and biophysical research communications.

[70]  L. Choo-Smith,et al.  Acceleration of Amyloid Fibril Formation by Specific Binding of Aβ-(1–40) Peptide to Ganglioside-containing Membrane Vesicles* , 1997, The Journal of Biological Chemistry.

[71]  P. Lansbury,et al.  Models of amyloid seeding in Alzheimer's disease and scrapie: mechanistic truths and physiological consequences of the time-dependent solubility of amyloid proteins. , 1997, Annual review of biochemistry.

[72]  Wei Hsu,et al.  The Mouse Fused Locus Encodes Axin, an Inhibitor of the Wnt Signaling Pathway That Regulates Embryonic Axis Formation , 1997, Cell.

[73]  U. Wagner,et al.  Overexpression of the mouse dishevelled‐1 protein inhibits GSK‐3β‐mediated phosphorylation of tau in transfected mammalian cells , 1997, FEBS letters.

[74]  Virginia M. Y. Lee,et al.  Lithium Reduces Tau Phosphorylation by Inhibition of Glycogen Synthase Kinase-3* , 1997, The Journal of Biological Chemistry.

[75]  P. S. Klein,et al.  Activation of the Wnt signaling pathway: a molecular mechanism for lithium action. , 1997, Developmental biology.

[76]  C. Finch,et al.  Aging, Metabolism, and Alzheimer Disease: Review and Hypotheses , 1997, Experimental Neurology.

[77]  N. Inestrosa,et al.  Acetylcholinesterase promotes the aggregation of amyloid-beta-peptide fragments by forming a complex with the growing fibrils. , 1997, Journal of molecular biology.

[78]  D. Miller,et al.  Quantitative neuronal c-Fos and c-Jun expression in Alzheimer’s disease1 1 To whom correspondence should be addressed. , 1998, Neurobiology of Aging.

[79]  T. Dale,et al.  Signal transduction by the Wnt family of ligands. , 1998, The Biochemical journal.

[80]  S. Singer,et al.  Specific intercellular binding of the beta-amyloid precursor protein to the presenilins induces intercellular signaling: its significance for Alzheimer's disease. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[81]  I. Greenwald,et al.  Effects of SEL-12 presenilin on LIN-12 localization and function in Caenorhabditis elegans. , 1998, Development.

[82]  M. Boutros,et al.  Dishevelled Activates JNK and Discriminates between JNK Pathways in Planar Polarity and wingless Signaling , 1998, Cell.

[83]  Hans Clevers,et al.  Destabilization of β-catenin by mutations in presenilin-1 potentiates neuronal apoptosis , 1998, Nature.

[84]  R. Nusse,et al.  Mechanisms of Wnt signaling in development. , 1998, Annual review of cell and developmental biology.

[85]  D. Borchelt,et al.  Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons , 1998, Neuron.

[86]  S Lovestone,et al.  Abnormalities of Wnt signalling in schizophrenia – evidence for neurodevelopmental abnormality , 1998, Neuroreport.

[87]  R. Tanzi,et al.  Monogenic determinants of familial Alzheimer's disease: presenilin-1 mutations , 1998, Cellular and Molecular Life Sciences CMLS.

[88]  P. Fraser,et al.  The Presenilin 1 Protein Is a Component of a High Molecular Weight Intracellular Complex That Contains β-Catenin* , 1998, The Journal of Biological Chemistry.

[89]  B. P. Doctor,et al.  Stable Complexes Involving Acetylcholinesterase and Amyloid-β Peptide Change the Biochemical Properties of the Enzyme and Increase the Neurotoxicity of Alzheimer’s Fibrils , 1998, The Journal of Neuroscience.

[90]  N. Perrimon,et al.  Differential Recruitment of Dishevelled Provides Signaling Specificity in the Planar Cell Polarity and Wingless Signaling Pathways in Drosophila, Planar Cell Polarity (pcp) Signaling Is Mediated by the Receptor Frizzled (fz) and Transduced by Dishevelled (dsh). Wingless (wg) Signaling Also Requires , 2022 .

[91]  Brian J Cummings,et al.  Plaque biogenesis in brain aging and Alzheimer’s disease. II. Progressive transformation and developmental sequence of dystrophic neurites , 1998, Acta Neuropathologica.

[92]  N. Robakis,et al.  Alzheimer's disease: a re-examination of the amyloid hypothesis , 1998, Trends in Neurosciences.

[93]  P. Lansbury,et al.  A detergent-insoluble membrance compartment contains Aβ in vivo , 1998, Nature Medicine.

[94]  I. Greenwald,et al.  LIN-12/Notch signaling: lessons from worms and flies. , 1998, Genes & development.

[95]  K. Kosik.  Presenilin Interactions and Alzheimer's Disease , 1998, Science.

[96]  D. Dickson,et al.  Mitotic phosphoepitopes precede paired helical filaments in Alzheimer’s disease , 1998, Neurobiology of Aging.

[97]  G. Schellenberg,et al.  Presenilin‐1 mutation alters NGF‐induced neurite outgrowth, calcium homeostasis, and transcription factor (AP‐1) activation in PC12 cells , 1998, Journal of neuroscience research.

[98]  D. Alkon,et al.  Alzheimer's-specific effects of soluble beta-amyloid on protein kinase C-alpha and -gamma degradation in human fibroblasts. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[99]  R. Terry.  The cytoskeleton in Alzheimer disease. , 1998, Journal of neural transmission. Supplementum.

[100]  J. Avila,et al.  Implication of cyclin‐dependent kinases and glycogen synthase kinase 3 in the phosphorylation of microtubule‐associated protein 1B in developing neuronal cells , 1998, Journal of neuroscience research.

[101]  R. Doms,et al.  Detection of a Novel Intraneuronal Pool of Insoluble Amyloid β Protein that Accumulates with Time in Culture , 1998, The Journal of cell biology.

[102]  Hugo Vanderstichele,et al.  Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.

[103]  Y. Ip,et al.  Signal transduction by the c-Jun N-terminal kinase (JNK)--from inflammation to development. , 1998, Current opinion in cell biology.

[104]  M. Tabaton,et al.  Amyloid‐β Deposition in Alzheimer Transgenic Mice Is Associated with Oxidative Stress , 1998, Journal of neurochemistry.

[105]  E. Mandelkow,et al.  Sequential phosphorylation of Tau by glycogen synthase kinase-3beta and protein kinase A at Thr212 and Ser214 generates the Alzheimer-specific epitope of antibody AT100 and requires a paired-helical-filament-like conformation. , 1998, European journal of biochemistry.

[106]  B. Hyman,et al.  Notch Is Expressed in Adult Brain, Is Coexpressed with Presenilin-1, and Is Altered in Alzheimer Disease , 1998, Journal of neuropathology and experimental neurology.

[107]  D. Selkoe,et al.  The cell biology of β-amyloid precursor protein and presenilin in Alzheimer's disease , 1998 .

[108]  N. Inestrosa,et al.  Laminin blocks the assembly of wild-type A beta and the Dutch variant peptide into Alzheimer's fibrils. , 1998, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.

[109]  V. Adler,et al.  JNK targets p53 ubiquitination and degradation in nonstressed cells. , 1998, Genes & development.

[110]  C. L. Harris,et al.  Stable Association of Presenilin Derivatives and Absence of Presenilin Interactions with APP , 1998, Neurobiology of Disease.

[111]  M. Mercken,et al.  Presenilin 1 associates with glycogen synthase kinase-3beta and its substrate tau. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[112]  Changiz Geula,et al.  Abnormalities of neural circuitry in Alzheimer's disease , 1998, Neurology.

[113]  E. Mandelkow,et al.  Tau in Alzheimer's disease. , 1998, Trends in cell biology.

[114]  J. Wands,et al.  P53- and CD95-associated apoptosis in neurodegenerative diseases. , 1998, Laboratory investigation; a journal of technical methods and pathology.

[115]  D. Chuang,et al.  Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats , 1998, Neuroreport.

[116]  A. Harris,et al.  Regulation of Wnt5a expression in human mammary cells by protein kinase C activity and the cytoskeleton. , 1998, British Journal of Cancer.

[117]  D. Israeli,et al.  Inhibition of presenilin 1 expression is promoted by p53 and p21WAF-1 and results in apoptosis and tumor suppression , 1998, Nature Medicine.

[118]  Bruce A. Yankner,et al.  Aging renders the brain vulnerable to amyloid β-protein neurotoxicity , 1998, Nature Medicine.

[119]  A. Takashima,et al.  Direct association of presenilin‐1 with β‐catenin , 1998 .

[120]  G. Schellenberg,et al.  Tau is a candidate gene for chromosome 17 frontotemporal dementia , 1998, Annals of neurology.

[121]  D. Borchelt.  Metabolism of Presenilin 1: Influence of Presenilin 1 on Amyloid Precursor Protein Processing , 1998, Neurobiology of Aging.

[122]  R. Moon,et al.  Wnt signaling: why is everything so negative? , 1998, Current opinion in cell biology.

[123]  Molecular Interactions of Acetylcholinesterase with the Synaptic Basal Lamina and the Senile Plaques , 1998 .

[124]  P. Greengard,et al.  Endoplasmic reticulum and trans-Golgi network generate distinct populations of Alzheimer beta-amyloid peptides. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[125]  J Mao,et al.  Dishevelled Proteins Lead to Two Signaling Pathways , 1999, The Journal of Biological Chemistry.

[126]  M. Frosch,et al.  Presenilin 1 Facilitates the Constitutive Turnover of β-Catenin: Differential Activity of Alzheimer’s Disease–Linked PS1 Mutants in the β-Catenin–Signaling Pathway , 1999, The Journal of Neuroscience.

[127]  R. Jope.  Anti-bipolar therapy: mechanism of action of lithium , 1999, Molecular Psychiatry.

[128]  N. Inestrosa,et al.  PC12 and neuro 2a cells have different susceptibilities to acetylcholinesterase–amyloid complexes, amyloid25–35 fragment, glutamate, and hydrogen peroxide , 1999, Journal of neuroscience research.

[129]  R. Nusse,et al.  WNT targets. Repression and activation. , 1999, Trends in genetics : TIG.

[130]  J. Ávila,et al.  Lithium protects cultured neurons against β‐amyloid‐induced neurodegeneration , 1999 .

[131]  R. Moon,et al.  Protein kinase C is differentially stimulated by Wnt and Frizzled homologs in aG-protein-dependent manner , 1999, Current Biology.

[132]  A. Goate,et al.  Evidence for a physical interaction between presenilin and Notch. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

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

[134]  S. Lincoln,et al.  A Loss of Function Mutation of Presenilin-2 Interferes with Amyloid β-Peptide Production and Notch Signaling* , 1999, The Journal of Biological Chemistry.

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

[136]  A. Ishimoto,et al.  Characterization of Mouse Dishevelled (Dvl) Proteins in Wnt/Wingless Signaling Pathway* , 1999, The Journal of Biological Chemistry.

[137]  Tsuyoshi Miyaoka,et al.  Increased expression of Wnt-1 in schizophrenic brains , 1999, Schizophrenia Research.

[138]  M. Mattson,et al.  Altered Calcium Homeostasis and Mitochondrial Dysfunction in Cortical Synaptic Compartments of Presenilin‐1 Mutant Mice , 1999, Journal of neurochemistry.

[139]  N. Inestrosa,et al.  Neurotoxicity of acetylcholinesterase amyloid β‐peptide aggregates is dependent on the type of Aβ peptide and the AChE concentration present in the complexes , 1999, FEBS letters.

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

[141]  D. Chuang,et al.  Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[142]  J. Morris,et al.  Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease , 1999, Annals of neurology.

[143]  D. Selkoe,et al.  Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.

[144]  R. Rozmahel,et al.  Presenilin mutations associated with Alzheimer disease cause defective intracellular trafficking of β-catenin,a component of the presenilin protein complex , 1999, Nature Medicine.