Cited by 2

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Low density lipoprotein increases amyloid precursor protein processing to amyloidogenic pathway in differentiated SH-SY5Y cells

Yamchuen, Panit, Jeenapongsa, Rattima, Nudmamud-Thanoi, Sutisa, Limpeanchob, Nanteetip·2017·Biologia

Overview

Integrity signals

Registry

Crossref · 10.1515/biolog-2017-0024

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

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

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, 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?

  • LDL exposure disrupts endolysosomal function in primary cortical neurons and neuronal cell lines.

    “In parallel, studies examining the effects of native (non‐oxidized) and oxidized LDL (ox‐LDL) on brain cells have reported that LDL exposure in primary cortical neurons and neuronal cell lines disrupts endolysosomal function, increases amyloid‐β production, reduces synaptophysin levels, and induces mitochondrial dysfunction and oxidative stress (Engel et al. 2016; Hui et al. 2012; Yamchuen et al.”
  • LDL exposure induces oxidative stress in primary cortical neurons and neuronal cell lines.

    “In parallel, studies examining the effects of native (non‐oxidized) and oxidized LDL (ox‐LDL) on brain cells have reported that LDL exposure in primary cortical neurons and neuronal cell lines disrupts endolysosomal function, increases amyloid‐β production, reduces synaptophysin levels, and induces mitochondrial dysfunction and oxidative stress (Engel et al. 2016; Hui et al. 2012; Yamchuen et al.”
  • LDL exposure induces mitochondrial dysfunction in primary cortical neurons and neuronal cell lines.

    “In parallel, studies examining the effects of native (non‐oxidized) and oxidized LDL (ox‐LDL) on brain cells have reported that LDL exposure in primary cortical neurons and neuronal cell lines disrupts endolysosomal function, increases amyloid‐β production, reduces synaptophysin levels, and induces mitochondrial dysfunction and oxidative stress (Engel et al. 2016; Hui et al. 2012; Yamchuen et al.”
  • LDL exposure reduces synaptophysin levels in primary cortical neurons and neuronal cell lines.

    “In parallel, studies examining the effects of native (non‐oxidized) and oxidized LDL (ox‐LDL) on brain cells have reported that LDL exposure in primary cortical neurons and neuronal cell lines disrupts endolysosomal function, increases amyloid‐β production, reduces synaptophysin levels, and induces mitochondrial dysfunction and oxidative stress (Engel et al. 2016; Hui et al. 2012; Yamchuen et al.”
  • LDL exposure increases amyloid-β production in primary cortical neurons and neuronal cell lines.

    “In parallel, studies examining the effects of native (non‐oxidized) and oxidized LDL (ox‐LDL) on brain cells have reported that LDL exposure in primary cortical neurons and neuronal cell lines disrupts endolysosomal function, increases amyloid‐β production, reduces synaptophysin levels, and induces mitochondrial dysfunction and oxidative stress (Engel et al. 2016; Hui et al. 2012; Yamchuen et al.”

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 26

  1. Bereczki E., Bernat G., Csont T., Ferdinandy P., Scheich H. & Santha M. 2008. Overexpression of human apolipoprotein B-100 induces severe neurodegeneration in transgenic mice. J. Proteome Res. 7: 2246–2252. · DOI · Paper page
  2. Bjelik A., Bereczki E., Gonda S., Juhasz A., Rimanoczy A., Zana M., Csont T., Pakaski M., Boda K., Ferdinandy P., Dux L., Janka Z., Santha M. & Kalman J. 2006. Human apoB overexpression and a high-cholesterol diet differently modify the brain APP metabolism in the transgenic mouse model of atherosclerosis. Neurochem. Int. 49: 393–400. · DOI
  3. Chasseigneaux S. & Allinquant B. 2012. Functions of Aβ, sAPPα and sAPPβ: similarities and differences. J. Neurochem. 120 (Suppl. 1): 99–108. · DOI
  4. Chen X., Hui L. & Geiger J.D. 2014. Role of LDL cholesterol and endolysosomes in amyloidogenesis and Alzheimer’s disease. J. Neurol. Neurophysiol. 5: 236. · DOI
  5. Chen X., Wagener J.F., Morgan D.H., Hui L., Ghribi O. & Geiger J.D. 2010. Endolysosome mechanisms associated with Alzheimer’s disease-like pathology in rabbits ingesting cholesterol-enriched diet. J. Alzheimers Dis. 22: 1289–1303. · DOI
  6. Dias I.H., Mistry J., Fell S., Reis A., Spickett C.M., Polidori M.C., Lip G.Y. & Griffiths H.R. 2014. Oxidized LDL lipids increase β-amyloid production by SH-SY5Y cells through glutathione depletion and lipid raft formation. Free Radic. Biol. Med. 75: 48–59. · DOI
  7. Gamba P., Testa G., Gargiulo S., Staurenghi E., Poli G. & Leonarduzzi G. 2015. Oxidized cholesterol as the driving force behind the development of Alzheimer’s disease. Front. Aging Neurosci. 7: 119. · DOI · Paper page
  8. Ghribi O., Larsen B., Schrag M. & Herman M.M. 2006. High cholesterol content in neurons increases BACE, β-amyloid, and phosphorylated tau levels in rabbit hippocampus. Exp. Neurol. 200: 460–467. · DOI · Paper page
  9. Hui L., Chen X. & Geiger J.D. 2012. Endolysosome involvement in LDL cholesterol-induced Alzheimer’s disease-like pathology in primary cultured neurons. Life Sci. 91: 1159–1168. · DOI · Paper page
  10. Imtiaz B., Tolppanen A.M., Kivipelto M. & Soininen H. 2014. Future directions in Alzheimer’s disease from risk factors to prevention. Biochem. Pharmacol. 88: 661–670. · DOI
  11. Kankaanpaa J., Turunen S.P., Moilanen V., Horkko S. & Remes A.M. 2009. Cerebrospinal fluid antibodies to oxidized LDL are increased in Alzheimer’s disease. Neurobiol. Dis. 33: 467–472. · DOI
  12. Keller J.N., Hanni K.B. & Markesbery W.R. 1999. Oxidized lowdensity lipoprotein induces neuronal death: implications for calcium, reactive oxygen species, and caspases. J. Neurochem. 72: 2601–2609. · DOI
  13. Koyama A., Stone K. & Yaffe K. 2013. Serum oxidized lowdensity lipoprotein level and risk of cognitive impairment in older women. Neurobiol. Aging 34: 634–635.e2. · DOI
  14. Lichtenthaler S.F. 2011. α-Secretase in Alzheimer’s disease: molecular identity, regulation and therapeutic potential. J. Neurochem. 116: 10–21. · DOI
  15. Marques F., Sousa J.C., Sousa N. & Palha J.A. 2013. Bloodbrain-barriers in aging and in Alzheimer’s disease. Mol. Neurodegener. 8: 38. · DOI
  16. Marwarha G. & Ghribi O. 2015. Does the oxysterol 27-hydroxycholesterol underlie Alzheimer’s disease–Parkinson’s disease overlap? Exp. Gerontol. 68: 13–18. · DOI
  17. Matsuura E., Hughes G.R.V. & Khamashta M.A. 2008. Oxidation of LDL and its clinical implication. Autoimmun. Rev. 7: 558–566. · DOI · Paper page
  18. Maulik M., Westaway D., Jhamandas J.H. & Kar S. 2013. Role of cholesterol in APP metabolism and its significance in Alzheimer’s disease pathogenesis. Mol. Neurobiol. 47: 37–63. · DOI
  19. Multhaup G., Huber O., Buee L. & Galas M.C. 2015. Amyloid precursor protein (APP) metabolites APP intracellular fragment (AICD), Aβ42, and tau in nuclear roles. J. Biol. Chem. 290: 23515–23522. · DOI
  20. Namba Y., Tsuchiya H. & Ikeda K. 1992. Apolipoprotein B immunoreactivity in senile plaque and vascular amyloids and neurofibrillary tangles in the brains of patients with Alzheimer’s disease. Neurosci. Lett. 134: 264–266. · DOI
  21. Nowicki M., Muller K., Serke H., Kosacka J., Vilser C., Ricken A. & Spanel-Borowski K. 2010a. Oxidized low-density lipoprotein (oxLDL)-induced cell death in dorsal root ganglion cell cultures depends not on the lectin-like oxLDL receptor-1 but on the toll-like receptor-4. J. Neurosci. Res. 88: 403–412. · DOI
  22. Nowicki M., Serke H., Kosacka J., Muller K. & Spanel-Borowski K. 2010b. Oxidized low-density lipoprotein (oxLDL) induces cell death in neuroblastoma and survival autophagy in schwannoma cells. Exp. Mol. Pathol. 89: 276–283. · DOI
  23. Poli G., Biasi F. & Leonarduzzi G. 2013. Oxysterols in the pathogenesis of major chronic diseases. Redox Biol. 1: 125–130. · DOI
  24. Reitz C. 2013. Dyslipidemia and the risk of Alzheimer’s disease. Curr. Atheroscler. Rep. 15: 307. · DOI · Paper page
  25. Xiong H., Callaghan D., Jones A., Walker D.G., Lue L.F., Beach T.G., Sue L.I., Woulfe J., Xu H., Stanimirovic D.B. & Zhang W. 2008. Cholesterol retention in Alzheimer’s brain is responsible for high β- and γ-secretase activities and Aβ production. Neurobiol. Dis. 29: 422–437. · DOI
  26. Yamchuen P., Aimjongjun S. & Limpeanchob N. 2014. Oxidized low density lipoprotein increases acetylcholinesterase activity correlating with reactive oxygen species production. Neurochem. Int. 78: 1–6. · DOI

Cited by

Sorted by citations

Metadata

Authors
Yamchuen, P., Jeenapongsa, R., Nudmamud-Thanoi, S., & Limpeanchob, N.
Venue
Biologia
Published
2017-02
Volume
72
Issue
2
Pages
238-244
ISSN
  • 0006-3088
  • 1336-9563
Cited by
2
References
2
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