CoChat
Sign Up
Cited by 42

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

Overexpression of Human Apolipoprotein B-100 Induces Severe Neurodegeneration in Transgenic Mice

Bereczki, Erika, Bernát, Gábor, Csont, Tamás, Ferdinandy, Péter, Scheich, Henning, Sántha, Miklós·2008·Journal of Proteome Research
DOI 10.1021/pr7006329
Open this paper in CoChat — free account

Abstract

Recent studies showed correlation between increased serum apolipoprotein B-100 (apoB-100) level and Alzheimer's disease. To reveal the possible role of apoB-100 in neurodegeneration, we analyzed the serum lipoprotein and cerebral protein profiles, amyloid plaque formation, apoptosis and brain morphology of transgenic mice overexpressing the human apoB-100 protein. Serum lipoprotein profile showed significant increase of the plasma triglyceride level, while no alteration in total cholesterol was detected. The antibody microarray experiment revealed upregulation of several cytoskeletal, neuronal proteins and proteins that belong to the mitogen activated protein kinase pathway, indicating active apoptosis in the brain. Histochemical experiments showed formation of amyloid plaques and extensive neuronal death. Biochemical changes severely affected brain morphology; a dramatic genotype-dependent enlargement of the third and lateral ventricles in the brain was detected. On the basis of earlier and present results, we conclude that overexpressed human apoB-100 protein significantly increases the level of serum lipids (triglyceride upon normal chow diet and cholesterol on cholesterol-rich diet) which leads to cerebrovascular lesions and subsequently induces apoptosis and neurodegeneration.

Overview

Integrity signals

Registry

Crossref · 10.1021/pr7006329

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?

  • This model is superior to previous hypercholesterolaemic models in which mice were only deficient in LDLRs, that had only mildly elevated LDL cholesterol levels and little atherosclerosis, or that were based exclusively on the overexpression of apoB100 and no alteration in plasma total cholesterol.

    “This model is superior to previous hypercholesterolaemic models in which mice were only deficient in LDLRs, that had only mildly elevated LDL cholesterol levels and little atherosclerosis [27], or that were based exclusively on the overexpression of apoB100 and no alteration in plasma total cholesterol [28].”

    From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [28]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 35

  1. Chan L., 1992, J. Biol. Chem., 267, 25621, 10.1016/S0021-9258(18)35646-1 · DOI
  2. Caramelli P., 1999, Acta Neurol. Scand., 100, 61, 10.1111/j.1600-0404.1999.tb00724.x · DOI · Paper page
  3. Sabbagh M., 2004, J. Alzheimer Dis., 6, 585, 10.3233/JAD-2004-6602 · DOI · Paper page
  4. Kuo Y. M., 1998, Biochem. Biophys. Res. Commun., 252, 711, 10.1006/bbrc.1998.9652 · DOI · Paper page
  5. Puglielli L., 2003, Nat. Neurosci., 6, 345, 10.1038/nn0403-345 · DOI · Paper page
  6. Ehehalt R., 2003, J. Cell. Biol., 160, 113, 10.1083/jcb.200207113 · DOI · Paper page
  7. Lutjohann D., 2000, J. Lipid Res., 41, 195, 10.1016/S0022-2275(20)32052-6 · DOI
  8. Burgess B. L., 2006, Neurobiol. Dis., 24, 114, 10.1016/j.nbd.2006.06.007 · DOI · Paper page
  9. Bjelik A., 2006, Neurochem. Int., 49, 393, 10.1016/j.neuint.2006.01.026 · DOI
  10. Csont T., 2007, Cardiovasc. Res., 76, 100, 10.1016/j.cardiores.2007.06.006 · DOI
  11. Callow M. J., 1994, Procl. Natl. Acad. Sci. U.S.A., 91, 2130, 10.1073/pnas.91.6.2130 · DOI
  12. Hennig J., 1986, Magn. Reson. Med., 3, 823, 10.1002/mrm.1910030602 · DOI
  13. Tian D. H., 2000, J. Neurosci., 20, 6478, 10.1523/JNEUROSCI.20-17-06478.2000 · DOI
  14. Saez T. E., 2004, In Vivo, 18, 275
  15. Esposito G., 2006, Life Sci., 78, 2707, 10.1016/j.lfs.2005.10.023 · DOI
  16. Van Eldik L. J., 1994, Biochim. Biophys. Acta, 1223, 398, 10.1016/0167-4889(94)90101-5 · DOI
  17. Saitoh T., 2003, Ann. N.Y. Acad. Sci., 695, 34, 10.1111/j.1749-6632.1993.tb23023.x · DOI
  18. Luth H. J., 2001, Brain Res., 91, 57, 10.1016/S0006-8993(01)02758-5 · DOI · Paper page
  19. Hartley D. M., 1999, J. Neurosci., 19, 8876, 10.1523/JNEUROSCI.19-20-08876.1999 · DOI · Paper page
  20. Pettegrew J. W., 1988, Arch. Neurol., 45, 1093, 10.1001/archneur.1988.00520340047010 · DOI
  21. Vardimon L., 2005, Isr. Med. Assoc. J., 2, 46
  22. Burbaeva G. S., 2005, Neurochem. Res., 30, 1443, 10.1007/s11064-005-8654-x · DOI
  23. Gunnersen D., 1999, Proc. Natl. Acad. Sci. U.S.A., 92, 11949
  24. Smith S. K. F., 2000, Mol. Brain Res., 78, 100, 10.1016/S0169-328X(00)00079-6 · DOI
  25. Yu Y. X., 2006, J. Cell. Sci., 119, 3776, 10.1242/jcs.03151 · DOI
  26. Terlecky S. R., 1992, J. Biol. Chem., 267, 9202, 10.1016/S0021-9258(19)50408-2 · DOI
  27. Yu F., 2005, Biochem. Biophys. Res. Commun., 331, 278, 10.1016/j.bbrc.2005.03.148 · DOI
  28. Moreno F. J., 1998, Mol. Cell. Biochem., 183, 201, 10.1023/A:1006807814580 · DOI
  29. Eiselein L., 2007, Am. J. Physiol.: Heart Circ. Physiol., 292, H2745
  30. Hamel E., 2008, Exp. Physiol., 93, 116, 10.1113/expphysiol.2007.038729 · DOI
  31. Kalaria R. N., 2008, Neurobiol. Aging
  32. Launer L. J., 2007, Neurobiol. Aging
  33. Stampfer M. J., 2006, J. Intern. Med., 260, 211, 10.1111/j.1365-2796.2006.01687.x · DOI
  34. de Leeuw F. E., 2000, Stroke, 31, 425, 10.1161/01.STR.31.2.425 · DOI
  35. Newman A. B., 2005, J. Am. Geriatr. Soc., 53, 1101, 10.1111/j.1532-5415.2005.53360.x · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Bereczki, E., Bernát, G., Csont, T., Ferdinandy, P., Scheich, H., & Sántha, M.
Affiliations
Institute of Biochemistry, Biological Research Center, Hungarian Academy of Sciences, P.O. Box 521, H-6701 Szeged, Hungary, Special Lab Non-Invasive Brain Imaging, Leibniz-Institute for Neurobiology, Brenneckestr. 6, D-39118 Magdeburg, Germany, and Cardiovascular Research Group, Department of Biochemistry, University of Szeged, Dóm tér 9. H-6720 Szeged, Hungary
Venue
Journal of Proteome Research
Publisher
American Chemical Society (ACS)
Published
2008-05-13
Volume
7
Issue
6
Pages
2246-2252
ISSN
  • 1535-3893
  • 1535-3907
DOI
10.1021/pr7006329
Cited by
42
References
1
Language
en

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