CoChat
Sign Up
Cited by 59

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

M1 muscarinic receptor activation protects neurons from β-amyloid toxicity. A role for Wnt signaling pathway

Farías, Ginny G., Godoy, Juan A., Hernández, Félix, Avila, Jesús, Fisher, Abraham, Inestrosa, Nibaldo C.·2004·Neurobiology of Disease
DOI 10.1016/j.nbd.2004.07.016
Open this paper in CoChat — free account

Abstract

Amyloid-beta-peptide (Abeta) deposits are one of the hallmark features of Alzheimer's disease. Signal transduction alterations are implicate in the neuronal responses to Abeta, which include neurotransmitter systems and pathways involved in the maintenance of the nervous system. In this context, we have recently found that Abeta-neurotoxicity triggers a loss of Wnt signaling. We report here that M1-acetylcholine-muscarinic-receptor (mAChR) activation protects neurons from Abeta-toxicity. Concomitant with this effect, a modulation of the Wnt signaling was observed. M1 mAChR activation inhibits glycogen-synthase-kinase-3beta (GSK-3beta) activity, stabilizes cytoplasmic and nuclear beta-catenin, and induces the expression of the Wnt target genes engrailed and cyclin-D1, reverting the switch off of the Wnt pathway caused by Abeta-toxicity. Neurons from mice that overexpress GSK-3beta allow us to establish that M1 mAChR stimulation leads to GSK-3beta inactivation. We conclude that the cross-talk between the muscarinic signaling and Wnt components underlie the neuroprotective effect of the M1 mAChR activation.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.nbd.2004.07.016

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • β-Amyloid can also increase the activity of the Wnt pathway inhibitor GSK3β, inducing neuronal apoptosis and increasing the neurotoxicity associated with β-amyloid.

    “β-Amyloid can also increase the activity of the Wnt pathway inhibitor GSK3β, inducing neuronal apoptosis and increasing the neurotoxicity associated with β-amyloid.17”

    From Canonical Wnt pathway and the LDL receptor superfamily in neuronal cholesterol homeostasis and function (2024) · cites this paper as [17]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 62

  1. Aberle, 1997, β-catenin is a target for the ubiquitin–proteasome pathway, EMBO J., 16, 3797, 10.1093/emboj/16.13.3797 · DOI
  2. Alvarez, 1998, Stable complexes involving acetylcholinesterase and amyloid-β peptide change the biochemical properties of the enzyme and increase the neurotoxicity of Alzheimer's fibrils, J. Neurosci., 18, 3213, 10.1523/JNEUROSCI.18-09-03213.1998 · DOI
  3. Alvarez, 2004, Wnt-3a overcomes β-amyloid toxicity in rat hippocampal neurons, Exp. Cell Res., 297, 186, 10.1016/j.yexcr.2004.02.028 · DOI
  4. Alvarez, 1997, Acetylcholinesterase promotes the aggregation of amyloid-β-peptide fragments by forming a complex with the growing fibrils, J. Mol. Biol., 272, 348, 10.1006/jmbi.1997.1245 · DOI
  5. Alvarez, 1999, Lithium protects cultured neurons against β-amyloid-induced neurodegeneration, J. FEBS Lett., 453, 260, 10.1016/S0014-5793(99)00685-7 · DOI
  6. Anagnostaras, 2003, Selective cognitive dysfunction in acetylcholine M1 muscarinic receptor mutant mice, Nat. Neurosci., 6, 51, 10.1038/nn992 · DOI
  7. Asghari, 1998, Differential effects of mood stabilizers on Fos/Jun proteins and AP-1 DNA binding activity in human neuroblastoma SH-SY5Y cells, Brain Res. Mol. Brain Res., 58, 95, 10.1016/S0169-328X(98)00107-7 · DOI
  8. Bijur, 2001, Proapoptotic stimuli induce nuclear accumulation of glycogen synthase kinase-3β, J. Biol. Chem., 276, 37436, 10.1074/jbc.M105725200 · DOI
  9. Bijur, 2000, Glycogen synthase kinase-3β facilitates staurosporine- and heat shock-induced apoptosis. Protection by lithium, J. Biol. Chem., 275, 7583, 10.1074/jbc.275.11.7583 · DOI
  10. Billin, 2000, β-catenin-histone deacetylase interactions regulate the transition of LEF1 from a transcriptional repressor to an activator, Mol. Cell. Biol., 20, 6882, 10.1128/MCB.20.18.6882-6890.2000 · DOI · Paper page
  11. Buxbaum, 1992, Cholinergic agonists and interleukin 1 regulate processing and secretion of the Alzheimer β/A4 amyloid protein precursor, Proc. Natl. Acad. Sci. U. S. A., 89, 10075, 10.1073/pnas.89.21.10075 · DOI
  12. Cáceres, 1984, MAP2 is localized to the dendrites of hippocampal neurons which develop in culture, Brain Res., 315, 314, 10.1016/0165-3806(84)90167-6 · DOI
  13. Caricasole, 2003, The Wnt pathway, cell-cycle activation and β-amyloid: novel therapeutic strategies in Alzheimer's disease?, Trends Pharmacol. Sci., 24, 233, 10.1016/S0165-6147(03)00100-7 · DOI
  14. Cook, 1996, Wingless inactivates glycogen synthase kinase-3 via an intracellular signalling pathway which involves a protein kinase C, EMBO J., 15, 4526, 10.1002/j.1460-2075.1996.tb00830.x · DOI
  15. Coyle, 1983, Alzheimer's disease: a disorder of cortical cholinergic innervation, Science, 219, 1184, 10.1126/science.6338589 · DOI
  16. De Ferrari, 2000, Wnt signaling function in Alzheimer's disease, Brain Res. Brain Res. Rev., 33, 1, 10.1016/S0165-0173(00)00021-7 · DOI
  17. De Ferrari, 2003, Activation of Wnt signaling rescues neurodegeneration and behavioral impairments induced by β-amyloid fibrils, Mol. Psychiatry, 8, 195, 10.1038/sj.mp.4001208 · DOI
  18. De Sarno, 2003, Muscarinic receptor activation protects cells from apoptotic effects of DNA damage, oxidative stress, and mitochondrial inhibition, J. Biol. Chem., 278, 11086, 10.1074/jbc.M212157200 · DOI
  19. Eglen, 2001, Therapeutic opportunities from muscarinic receptor research, Trends Pharmacol. Sci., 22, 409, 10.1016/S0165-6147(00)01737-5 · DOI
  20. Fisher, 2000, Therapeutic strategies in Alzheimer's disease: M1 muscarinic agonists, Jpn. J. Pharmacol., 84, 101, 10.1254/jjp.84.101 · DOI
  21. Fisher, 2002, AF150(S) and AF267B: M1 muscarinic agonists as innovative therapies for Alzheimer's disease, J. Mol. Neurosci., 19, 145, 10.1007/s12031-002-0025-3 · DOI
  22. Fisher, 2003, M1 muscarinic agonists can modulate major hallmarks in Alzheimer's disease: implications in future therapy, J. Mol. Neurosci., 20, 139, 10.1385/JMN:20:3:349 · DOI
  23. Garrido, 2002, Protein kinase C inhibits amyloid β peptide neurotoxicity by acting on members of the Wnt pathway, FASEB J., 16, 1982, 10.1096/fj.02-0327fje · DOI
  24. Genis, 1999, Site-specific dephosphorylation of tau of apolipoprotein E-deficient and control mice by M1 muscarinic agonist treatment, J. Neurochem., 72, 206, 10.1046/j.1471-4159.1999.0720206.x · DOI
  25. Goode, 1992, Differential regulation of glycogen synthase kinase-3β by protein kinase C isotypes, J. Biol. Chem., 267, 16878, 10.1016/S0021-9258(18)41866-2 · DOI
  26. Gu, 2003, Activation of muscarinic receptors inhibits β-amyloid peptide-induced signaling in cortical slices, J. Biol. Chem., 278, 17546, 10.1074/jbc.M209892200 · DOI
  27. Haring, 1998, Mitogen-activated protein kinase-dependent and protein kinase C-dependent pathways link the m1 muscarinic receptor to β-amyloid precursor protein secretion, J. Neurochem., 71, 2094, 10.1046/j.1471-4159.1998.71052094.x · DOI · Paper page
  28. Hernandez, 2002, Spatial learning deficit in transgenic mice that conditionally over-express GSK-3β in the brain but do not form tau filaments, J. Neurochem., 83, 1529, 10.1046/j.1471-4159.2002.01269.x · DOI · Paper page
  29. Huber, 1996, Nuclear localization of β-catenin by interaction with transcription factor LEF-1, Mech. Dev., 59, 3, 10.1016/0925-4773(96)00597-7 · DOI
  30. Inestrosa, 1996, Acetylcholinesterase accelerates assembly of amyloid-β-peptides into Alzheimer's fibrils: possible role of the peripheral site of the enzyme, Neuron, 16, 881, 10.1016/S0896-6273(00)80108-7 · DOI
  31. Inestrosa, 2000, Acetylcholinesterase-amyloid-β-peptide interaction and Wnt signaling involvement in Abeta neurotoxicity, Acta Neurol. Scand., Suppl., 176, 53, 10.1034/j.1600-0404.2000.00308.x · DOI
  32. Inestrosa, 2004, Acetylcholinesterase (AChE)–amyloid-β-peptide complexes in Alzheimer's Disease. The Wnt signaling pathway, Curr. Alzheimer's Res., 10.2174/1567205043332063 · DOI
  33. Joyce, 1989, Regulation of muscarinic receptor in hippocampus following cholinergic denervation and reinnervation by septal and striatal transplants, J. Neurosci., 9, 2776, 10.1523/JNEUROSCI.09-08-02776.1989 · DOI
  34. Kaufer, 1998, Acute stress facilitates long-lasting changes in cholinergic gene expression, Nature, 393, 373, 10.1038/30741 · DOI · Paper page
  35. Kim, 1997, Phospholipase C isozymes selectively couple to specific neurotransmitter receptors, Nature, 389, 290, 10.1038/38508 · DOI · Paper page
  36. Leloup, 2000, M1 muscarinic receptors block caspase activation by phosphoinositide 3-kinase- and MAPK/ERK-independent pathways, Cell Death Differ., 7, 825, 10.1038/sj.cdd.4400713 · DOI
  37. Levey, 1996, Muscarinic acetylcholine receptor expression in memory circuits: implications for treatment of Alzheimer disease, Proc. Natl. Acad. Sci. U. S. A., 93, 13541, 10.1073/pnas.93.24.13541 · DOI
  38. Levey, 1995, Expression of m1-m4 muscarinic acetylcholine receptor proteins in rat hippocampus and regulation by cholinergic innervation, J. Neurosci., 15, 4077, 10.1523/JNEUROSCI.15-05-04077.1995 · DOI
  39. Lin, 1999, Cognitive changes and modified processing of amyloid precursor protein in the cortical and hippocampal system after cholinergic synapse loss and muscarinic receptor activation, Proc. Natl. Acad. Sci. U. S. A., 96, 12108, 10.1073/pnas.96.21.12108 · DOI
  40. Lucas, 2001, Decreased nuclear β-catenin, tau hyperphosphorylation and neurodegeneration in GSK-3β conditional transgenic mice, EMBO J., 20, 27, 10.1093/emboj/20.1.27 · DOI
  41. Ma, 2003, Muscarinic potentiation of GABA(A) receptor currents is gated by insulin signaling in the prefrontal cortex, J. Neurosci., 23, 1159, 10.1523/JNEUROSCI.23-04-01159.2003 · DOI · Paper page
  42. McGrew, 1999, Direct regulation of the Xenopus engrailed-2 promoter by the Wnt signaling pathway, and a molecular screen for Wnt-responsive genes, confirm a role for Wnt signaling during neural patterning in Xenopus, Mech. Dev., 87, 21, 10.1016/S0925-4773(99)00136-7 · DOI
  43. Merritt, 1997, Different sensitivities of neutrophil responses to a selective protein kinase C inhibitor Ro 31-8425; redundancy in signal transduction, Cell Signalling, 9, 53, 10.1016/S0898-6568(96)00097-6 · DOI
  44. Mudher, 2002, Alzheimer's disease-do tauists and baptists finally shake hands?, Trends Neurosci., 25, 22, 10.1016/S0166-2236(00)02031-2 · DOI
  45. Nitsch, 1992, Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors, Science, 258, 304, 10.1126/science.1411529 · DOI · Paper page
  46. Nitsch, 1998, Muscarinic acetylcholine receptors activate the acetylcholinesterase gene promoter, J. Physiol. (Paris), 92, 257, 10.1016/S0928-4257(98)80029-6 · DOI
  47. Nusse, 1997, A versatile transcriptional effector of Wingless signaling, Cell, 89, 321, 10.1016/S0092-8674(00)80210-X · DOI
  48. Nusse, 1992, Wnt genes, Cell, 69, 1073, 10.1016/0092-8674(92)90630-U · DOI
  49. Palmer, 2002, Pharmacotherapy for Alzheimer's disease: progress and prospects, Trends Pharmacol. Sci., 23, 426, 10.1016/S0165-6147(02)02056-4 · DOI
  50. Patapoutian, 2000, Roles of Wnt proteins in neural development and maintenance, Curr. Opin. Neurobiol., 10, 392, 10.1016/S0959-4388(00)00100-8 · DOI
  51. Reyes, 2004, Acetylcholinesterase–Abeta complexes are more toxic than abeta fibrils in rat hippocampus: effect on rat beta-amyloid aggregation, laminin expression, reactive astrocytosis, and neuronal cell loss, Am. J. Pathol., 164, 2163, 10.1016/S0002-9440(10)63774-1 · DOI
  52. Sadot, 1996, Activation of m1 muscarinic acetylcholine receptor regulates tau phosphorylation in transfected PC12 cells, J. Neurochem., 66, 877, 10.1046/j.1471-4159.1996.66020877.x · DOI
  53. Selkoe, 2001, Alzheimer's disease: genes, proteins, and therapy, Physiol. Rev., 81, 741, 10.1152/physrev.2001.81.2.741 · DOI · Paper page
  54. Shaw, 1997, Further evidence that the inhibition of glycogen synthase kinase-3β by IGF-1 is mediated by PDK1/PKB-induced phosphorylation of Ser-9 and not by dephosphorylation of Tyr-216, FEBS Lett., 416, 307, 10.1016/S0014-5793(97)01235-0 · DOI
  55. Sheldahl, 1999, Protein kinase C is differentially stimulated by Wnt and Frizzled homologs in a G-protein-dependent manner, Curr. Biol., 9, 695, 10.1016/S0960-9822(99)80310-8 · DOI
  56. Simantov, 1989, Selective regulation of different muscarinic receptors in septum and hippocampus neuronal cultures, Brain Res., 505, 160, 10.1016/0006-8993(89)90130-3 · DOI
  57. Takashima, 1993, Tau protein kinase I is essential for amyloid β-protein-induced neurotoxicity, Proc. Natl. Acad. Sci. U. S. A., 90, 7789, 10.1073/pnas.90.16.7789 · DOI
  58. Tetsu, 1999, β-catenin regulates expression of cyclin D1 in colon carcinoma cells, Nature, 398, 422, 10.1038/18884 · DOI · Paper page
  59. Xie, 2000, Protein kinase C iota protects neural cells against apoptosis induced by amyloid beta-peptide, Brain Res. Mol. Brain. Res., 82, 107, 10.1016/S0169-328X(00)00187-X · DOI
  60. Yankner, 1996, Mechanisms of neuronal degeneration in Alzheimer's disease, Neuron, 16, 921, 10.1016/S0896-6273(00)80115-4 · DOI
  61. Zhang, 1998, Destabilization of β-catenin by mutations in presenilin-1 potentiates neuronal apoptosis, Nature, 395, 698, 10.1038/27208 · DOI
  62. Zhang, 2003, Inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3) in response to lithium. Evidence for autoregulation of GSK-3, J. Biol. Chem., 29, 33067, 10.1074/jbc.M212635200 · DOI

Cited by

Sorted by citations

Metadata

Authors
Farías, G. G., Godoy, J. A., Hernández, F., Avila, J., Fisher, A., & Inestrosa, N. C.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2004-11
Volume
17
Issue
2
Pages
337-348
ISSN
0969-9961
DOI
10.1016/j.nbd.2004.07.016
Cited by
59
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review