CoChat
Sign Up
Cited by 656

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the β-amyloid precursor protein

Mattson, Mark P., Cheng, Bin, Culwell, Alan R., Esch, Fred S., Lieberburg, Ivan, Rydel, Russell E.·1993·Neuron
DOI 10.1016/0896-6273(93)90315-i
Open this paper in CoChat — free account

Abstract

The beta-amyloid precursor protein (beta APP) is a membrane-spanning glycoprotein that is the source of the beta-amyloid peptide (beta AP) which accumulates as senile plaques in the brains of patients with Alzheimer's disease. beta APP is normally processed such that a cleavage occurs within the beta AP, liberating secreted forms of beta APP (APPss) from the cell. The neuronal functions of these forms are unknown. We now report that APPss have a potent neuroprotective action in cultured rat hippocampal and septal neurons and in human cortical neurons. APPs695 and APPs751 protected neurons against hypoglycemic damage, and the neuroprotection was abolished by antibodies to a specific region common to both APPs695 and APPs751. APPss caused a rapid and prolonged reduction in [Ca2+]i and prevented the rise in [Ca2+]i that normally mediated hypoglycemic damage. APPss also protected neurons against glutamate neurotoxicity, effectively raising the excitotoxic threshold. APPss may normally play excitoprotective and neuromodulatory roles. Alternative processing of APPss in Alzheimer's disease may contribute to neuronal degeneration by compromising the normal function of APPss and by promoting the deposition of beta AP.

Overview

Integrity signals

Registry

Crossref · 10.1016/0896-6273(93)90315-i

Cites

6 of 6 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?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 67

  1. Abe, 1991, Selective induction of Kunitz-type inhibitor domain-containing amyloid precursor protein mRNA after persistent focal ischemia in rat cerebral cortex, Neurosci. Lett., 125, 172, 10.1016/0304-3940(91)90020-T · DOI
  2. Araki, 1992, Trophic effect of β-amyloid precursor protein on cerebral cortical neurons in culture, Biochem. Biophys. Res. Commun., 181, 265, 10.1016/S0006-291X(05)81412-3 · DOI
  3. Breen, 1991, Beta amyloid precursor protein mediates neuronal cell-cell and cell-surface adhesion, J. Neurosci. Res., 28, 90, 10.1002/jnr.490280109 · DOI
  4. Busciglio, 1992, Methodological variables in the assessment of beta amyloid neurotoxicity, Neurobiol. Aging, 13, 609, 10.1016/0197-4580(92)90065-6 · DOI
  5. Chen, 1991, An antibody to β amyloid and the amyloid precursor protein inhibits cell-substratum adhesion in many mammalian cell types, Neurosci. Lett., 125, 223, 10.1016/0304-3940(91)90034-Q · DOI
  6. Cheng, 1991, NGF and bFGF protect rat hippocampal and human cortical neurons against hypoglycemic damage by stabilizing calcium homeostasis, Neuron, 7, 1031, 10.1016/0896-6273(91)90347-3 · DOI
  7. Cheng, 1992, IGF-I and IGF-II protect cultured hippocampal and septal neurons against calcium-mediated hypoglycemic damage, J. Neurosci., 12, 1558, 10.1523/JNEUROSCI.12-04-01558.1992 · DOI
  8. Cheng, 1992, Glucose deprivation elicits neurofibrillary tangle-like antigenic changes in hippocampal neurons: prevention by NGF and bFGF, Exp. Neurol., 117, 114, 10.1016/0014-4886(92)90120-F · DOI
  9. Choi, 1988, Glutamate neurotoxicity and diseases of the nervous system, Neuron, 1, 623, 10.1016/0896-6273(88)90162-6 · DOI
  10. Dyrks, 1988, Identification, transmembrane orientation and biogenesis of the amyloid A4 precursor of Alzheimer's disease, EMBO J., 7, 949, 10.1002/j.1460-2075.1988.tb02900.x · DOI
  11. Elliott, 1993, Corticosterone exacerbates kainate-induced alterations in hippocampal tau immunoreactivity and spectrin proteolysis in vivo, J. Neurochem., 10.1111/j.1471-4159.1993.tb03537.x · DOI
  12. Esch, 1990, Cleavage of amyloid β peptide during constitutive processing of its precursor, Science, 248, 1122, 10.1126/science.2111583 · DOI
  13. Finklestein, 1988, Increased basic fibroblast growth factor (bFGF) immunoreactivity at the site of focal brain wounds, Brain Res., 460, 253, 10.1016/0006-8993(88)90370-8 · DOI
  14. Fukuchi, 1992, Increased expression of β-amyloid protein precursor and microtubule-associated protein tau during the differentiation of murine embryonal carcinoma cells, J. Neurochem., 58, 1863, 10.1111/j.1471-4159.1992.tb10063.x · DOI
  15. Gibson, 1987, Calcium and the aging nervous system, Neurobiol. Aging, 8, 329, 10.1016/0197-4580(87)90072-8 · DOI
  16. Golde, 1992, Processing of the amyloid protein precursor to potentially amyloidogenic derivatives, Science, 255, 728, 10.1126/science.1738847 · DOI
  17. Greenamyre, 1989, Excitatory amino acids and Alzheimer's disease, Neurobiol. Aging, 10, 593, 10.1016/0197-4580(89)90143-7 · DOI
  18. Grynkiewicz, 1985, A new generation of calcium indicators with greatly improved fluorescence properties, J. Biol. Chem., 260, 3440, 10.1016/S0021-9258(19)83641-4 · DOI
  19. Haass, 1991, Processing of β-amyloid precursor protein in microglia and astrocytes favors an internal localization over constitutive secretion, J. Neurosci., 11, 3783, 10.1523/JNEUROSCI.11-12-03783.1991 · DOI
  20. Henriksson, 1991, Analysis and quantitation of the β-amyloid precursor protein in the cerebrospinal fluid of Alzheimer's disease patients with a monoclonal antibody-based immunoassay, J. Neurochem., 56, 1037, 10.1111/j.1471-4159.1991.tb02026.x · DOI
  21. Hoyer, 1988, Glucose metabolism as the site of the primary abnormality in early-onset dementia of Alzheimer type?, J. Neurol., 235, 143, 10.1007/BF00314304 · DOI
  22. Jagust, 1991, Diminished glucose transport in Alzheimer's disease: dynamic PET studies, J. Cereb. Blood Flow Metab., 11, 323, 10.1038/jcbfm.1991.65 · DOI
  23. Johnson-Wood, 1990, Identification of specific binding sites for 125I secreted APP751 on intact fibroblast cells, Neurobiol. Aging, 11, 306, 10.1016/0197-4580(90)90774-T · DOI
  24. Kalaria, 1989, Reduced glucose transporter at the blood-brain barrier and in cerebral cortex in Alzheimer's disease, J. Neurochem., 53, 1083, 10.1111/j.1471-4159.1989.tb07399.x · DOI · Paper page
  25. Kametani, 1990, Amyloid β-protein precursor (APP) of cultured cells: secretory and non-secretory forms of APP, J. Neurol. Sci., 97, 43, 10.1016/0022-510X(90)90097-7 · DOI
  26. Kater, 1988, Calcium regulation of the neuronal growth cone, Trends Neurosci., 11, 315, 10.1016/0166-2236(88)90094-X · DOI
  27. Kawarabayashi, 1991, Expression of APP in the early stage of brain damage, Brain Res., 563, 334, 10.1016/0006-8993(91)91558-I · DOI
  28. Kennedy, 1989, Regulation of synaptic transmission in the central nervous system: long-term potentiation, Cell, 59, 777, 10.1016/0092-8674(89)90601-6 · DOI
  29. Kitaguchi, 1990, Enzyme specificity of proteinase inhibitor region in amyloid precursor protein of Alzheimer's disease: different properties compared with protease nexin I, Biochim. Biophys. Acta, 1038, 105, 10.1016/0167-4838(90)90017-A · DOI
  30. Koh, 1990, β-Amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage, Brain Res., 533, 315, 10.1016/0006-8993(90)91355-K · DOI
  31. Lorez, 1989, Nerve growth factor increases in adult rat brain after hypoxic injury, Neurosci. Lett., 98, 339, 10.1016/0304-3940(89)90425-4 · DOI
  32. Mattson, 1990, Antigenic changes similar to those seen in neurofibrillary tangles are elicited by glutamate and Ca2+ influx in cultured hippocampal neurons, Neuron, 4, 105, 10.1016/0896-6273(90)90447-N · DOI
  33. Mattson, 1992, Calcium as sculptor and destroyer of neural circuitry, Exp. Gerontol., 27, 29, 10.1016/0531-5565(92)90027-W · DOI
  34. Mattson, 1988, Isolated hippocampal neurons in cryopreserved long-term cultures: development of neuro-architecture and sensitivity to NMDA, Int.J. Dev. Neurosci., 6, 439, 10.1016/0736-5748(88)90050-0 · DOI
  35. Mattson, 1990, Cell culture of cryopreserved human fetal cerebral cortical and hippocampal neurons: neuronal development and responses to tropic factors, Brain Res., 522, 204, 10.1016/0006-8993(90)91462-P · DOI
  36. Mattson, 1992, β-Amyloid precursor protein and Alzheimer's disease: the peptide plot thickens, Neurobiol. Aging, 13, 617, 10.1016/0197-4580(92)90068-9 · DOI
  37. Mattson, 1988, Intracellular messengers in the generation and degeneration of hippocampal neuroarchitecture, J. Neurosci. Res., 21, 447, 10.1002/jnr.490210236 · DOI
  38. Mattson, 1989, Fibroblast growth factor and glutamate: opposing roles in the generation and degeneration of hippocampal neuroarchitecture, J. Neurosci., 9, 3728, 10.1523/JNEUROSCI.09-11-03728.1989 · DOI · Paper page
  39. Mattson, 1991, Effects of elevated intracellular calcium levels on the cytoskeleton and tau in cultured human cerebral cortical neurons, Mol. Chem. Neuropathol., 15, 117, 10.1007/BF03159951 · DOI
  40. Mattson, 1992, β-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity, J. Neurosci., 12, 376, 10.1523/JNEUROSCI.12-02-00376.1992 · DOI
  41. Milward, 1992, The amyloid protein precursor of Alzheimer's disease is a mediator of the effects of nerve growth factor on neurite outgrowth, Neuron, 9, 129, 10.1016/0896-6273(92)90228-6 · DOI
  42. Monyer, 1989, Glucose deprivation neuronal injury in cortical culture, Brain Res., 483, 347, 10.1016/0006-8993(89)90179-0 · DOI
  43. Nakamura, 1992, Amyloid β-protein precursor deposition in rat hippocampus lesioned by ibotenic acid injection, Neurosci. Lett., 136, 95, 10.1016/0304-3940(92)90656-R · DOI
  44. Ohgami, 1992, Alzheimer's amyloid precursor protein accumulates within axonal swellings in human brain lesions, Neurosci. Lett., 136, 75, 10.1016/0304-3940(92)90651-M · DOI
  45. Oltersdorf, 1989, The secreted form of Alzheimer's amyloid precursor protein with the Kunitz domain is protease nexin II, Nature, 341, 144, 10.1038/341144a0 · DOI
  46. Oltersdorf, 1990, The Alzheimer amyloid precursor protein, J. Biol. Chem., 265, 4492, 10.1016/S0021-9258(19)39590-0 · DOI
  47. Otsuka, 1991, Rapid appearance of β-amyloid precursor protein immunoreactivity in damaged axons and reactive glial cells in rat brain following needle stab injury, Brain Res., 568, 335, 10.1016/0006-8993(91)91422-W · DOI
  48. Pike, 1991, In vitro aging of β-amyloid protein causes peptide aggregation and neurotoxicity, Brain Res., 563, 311, 10.1016/0006-8993(91)91553-D · DOI
  49. Quon, 1990, Fibroblast growth factor induces beta-amyloid precursor mRNA in glial but not neuronal cultured cells, Biochem. Biophys. Res. Commun., 167, 96, 10.1016/0006-291X(90)91735-B · DOI
  50. Roberts, 1991, βA4 amyloid protein deposition in brain after head injury, Lancet, 338, 1422, 10.1016/0140-6736(91)92724-G · DOI
  51. Roch, 1992, Bacterial expression, purification, and functional mapping of the amyloid β/A4 protein precursor, J. Biol. Chem., 267, 2214, 10.1016/S0021-9258(18)45864-4 · DOI
  52. Saitoh, 1989, Secreted form of amyloid β protein precursor is involved in the growth regulation of fibroblasts, Cell, 58, 615, 10.1016/0092-8674(89)90096-2 · DOI
  53. Salbaum, 1988, The promoter of Alzheimer's disease amyloid A4 precursor gene, EMBO J., 7, 2807, 10.1002/j.1460-2075.1988.tb03136.x · DOI
  54. Schubert, 1989, Amyloid beta protein precursor is a mitogen, Biochem. Biophys. Res. Common., 162, 83, 10.1016/0006-291X(89)91965-7 · DOI
  55. Schubert, 1989, The regulation of amyloid β protein precursor secretion and its modulatory role in cell adhesion, Neuron, 3, 689, 10.1016/0896-6273(89)90237-7 · DOI
  56. Schubert, 1991, Localization of Alzheimer βA4 amyloid precursor protein at cell and peripheral synaptic sites, Brain Res., 563, 184, 10.1016/0006-8993(91)91532-6 · DOI
  57. Selkoe, 1989, Biochemistry of altered brain proteins in Alzheimer's disease, Annu. Rev. Neurosci., 12, 463, 10.1146/annurev.ne.12.030189.002335 · DOI
  58. Seubert, 1993, Secretion of β-amyloid precursor protein cleaved at the amino terminus of the β-amyloid peptide, Nature, 361, 260, 10.1038/361260a0 · DOI
  59. Siesjo, 1989, Calcium, excitotoxins, and neuronal death in the brain, Ann. NY Acad. Sci., 568, 234, 10.1111/j.1749-6632.1989.tb12513.x · DOI
  60. Sims, 1990, Altered glucose metabolism in Alzheimer's disease, Ann. Neurol., 27, 691, 10.1002/ana.410270621 · DOI
  61. Sinha, 1990, The protease inhibitory properties of the Alzheimer's β-amyloid precursor protein, J. Biol. Chem., 265, 8983, 10.1016/S0021-9258(19)38798-8 · DOI
  62. Sisodia, 1990, Evidence that beta-amyloid protein in Alzheimer's disease is not derived by normal processing, Science, 248, 492, 10.1126/science.1691865 · DOI
  63. Smith, 1990, Platelet coagulation factor Xla-inhibitor, a form of Alzheimer amyloid precursor protein, Science, 248, 1126, 10.1126/science.2111585 · DOI
  64. Spillantini, 1989, Expression and cellular localization of amyloid β-protein precursor transcripts in normal human brain and in Alzheimer's disease, Mol. Brain Res., 6, 143, 10.1016/0169-328X(89)90048-X · DOI
  65. Van Nostrand, 1989, Protease nexin-II, a potent antichymotrypsin, shows identity to amyloid beta-protein precursor, Nature, 341, 546, 10.1038/341546a0 · DOI
  66. Van Nostrand, 1990, Immunopurification and protease inhibitory properties of protease nexin-2/amyloid β-protein precursor, J. Biol. Chem., 265, 9591, 10.1016/S0021-9258(19)38706-X · DOI
  67. Wieloch, 1985, Hypoglycemia-induced neuronal damage prevented by an N-methyl-d-aspartate antagonist, Science, 230, 681, 10.1126/science.2996146 · DOI

Cited by

Sorted by citations

Metadata

Authors
Mattson, M. P., Cheng, B., Culwell, A. R., Esch, F. S., Lieberburg, I., & Rydel, R. E.
Venue
Neuron
Publisher
Elsevier BV
Published
1993-02
Volume
10
Issue
2
Pages
243-254
ISSN
0896-6273
DOI
10.1016/0896-6273(93)90315-i
Cited by
656
References
6
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