The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer’s Disease Mutations
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
C83 is a preferential substrate of γ-secretase and the most abundant APP fragment in cultured neurons.
“consistent with C83 being a preferential substrate of γ-secretase [32] and the most abundant APP fragment in cultured neurons [15, 16]”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Zhang, Y., Chen, K., Sloan, S. A., Bennett, M. L., Scholze, A. R., O'Keeffe, S., Phatnani, H. P., Guarnieri, P., Caneda, C., Ruderisch, N., et al. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.1860-14.2014 · Cited by 4,875
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., Chi, H., Lin, C., Li, G., Holman, K., et al. (1995) · Nature · doi:10.1038/375754a0 · Cited by 4,051
Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells
Israel, M. A., Yuan, S. H., Bardy, C., Reyna, S. M., Mu, Y., Herrera, C., Hefferan, M. P., Van Gorp, S., Nazor, K. L., Boscolo, F. S., et al. (2012) · Nature · doi:10.1038/nature10821 · Cited by 1,253
Self-citationapoE isoform–specific disruption of amyloid β peptide clearance from mouse brain
Deane, R., Sagare, A., Hamm, K., Parisi, M., Lane, S., Finn, M. B., Holtzman, D. M., & Zlokovic, B. V. (2008) · Journal of Clinical Investigation · doi:10.1172/jci36663 · Cited by 771
Treusch, S., Hamamichi, S., Goodman, J. L., Matlack, K. E. S., Chung, C. Y., Baru, V., Shulman, J. M., Parrado, A., Bevis, B. J., Valastyan, J. S., et al. (2011) · Science · doi:10.1126/science.1213210 · Cited by 379
Amyloid accelerates tau propagation and toxicity in a model of early Alzheimer’s disease
Pooler, A. M., Polydoro, M., Maury, E. A., Nicholls, S. B., Reddy, S. M., Wegmann, S., William, C., Saqran, L., Cagsal-Getkin, O., Pitstick, R., et al. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0199-x · Cited by 236
Pietrzik, C. U., Busse, T., Merriam, D. E., Weggen, S., & Koo, E. H. (2002) · The EMBO Journal · doi:10.1093/emboj/cdf568 · Cited by 198
Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β
Vossel, K. A., Xu, J. C., Fomenko, V., Miyamoto, T., Suberbielle, E., Knox, J. A., Ho, K., Kim, D. H., Yu, G.-Q., & Mucke, L. (2015) · Journal of Cell Biology · doi:10.1083/jcb.201407065 · Cited by 167
More than cholesterol transporters: lipoprotein receptors in CNS function and neurodegeneration
Lane-Donovan, C., Philips, G. T., & Herz, J. (2014) · Neuron · doi:10.1016/j.neuron.2014.08.005 · Cited by 158
Amyloid precursor protein-induced axonopathies are independent of amyloid-β peptides
Stokin, G. B., Almenar-Queralt, A., Gunawardena, S., Rodrigues, E. M., Falzone, T., Kim, J., Lillo, C., Mount, S. L., Roberts, E. A., McGowan, E., et al. (2008) · Human Molecular Genetics · doi:10.1093/hmg/ddn240 · Cited by 72 · cited 1×
“These types of defects 770 Cell Reports 17, 759–773, October 11, 2016 could lead to previously reported axonal amyloid-dependent and -independent transport defects (Kim et al., 2015; Stokin et al., 2008; Vossel et al., 2015).”
Self-citation
Flagged first, then by citations
Research works printed but not linked: 57
- 2014, 2014 Alzheimer’s disease facts and figures, Alzheimers Dement, 10, e47
- Anderson, 2005, Transcytosis of NgCAM in epithelial cells reflects differential signal recognition on the endocytic and secretory pathways, J. Cell Biol., 170, 595, 10.1083/jcb.200506051 · DOI
- Ascaño, 2009, Axonal targeting of Trk receptors via transcytosis regulates sensitivity to neurotrophin responses, J. Neurosci., 29, 11674, 10.1523/JNEUROSCI.1542-09.2009 · DOI
- Barres, 2001, Cholesterol—making or breaking the synapse, Science, 294, 1296, 10.1126/science.1066724 · DOI
- Buggia-Prévot, 2014, Axonal BACE1 dynamics and targeting in hippocampal neurons: a role for Rab11 GTPase, Mol. Neurodegener., 9, 1, 10.1186/1750-1326-9-1 · DOI
- Burns, 2003, Presenilin redistribution associated with aberrant cholesterol transport enhances beta-amyloid production in vivo, J. Neurosci., 23, 5645, 10.1523/JNEUROSCI.23-13-05645.2003 · DOI
- Cai, 2003, Presenilin-1 regulates intracellular trafficking and cell surface delivery of β-amyloid precursor protein, J. Biol. Chem., 278, 3446, 10.1074/jbc.M209065200 · DOI
- Cataldo, 2000, Endocytic pathway abnormalities precede amyloid β deposition in sporadic Alzheimer’s disease and Down syndrome: differential effects of APOE genotype and presenilin mutations, Am. J. Pathol., 157, 277, 10.1016/S0002-9440(10)64538-5 · DOI · Paper page
- Cataldo, 2001, Endocytic disturbances distinguish among subtypes of Alzheimer’s disease and related disorders, Ann. Neurol., 50, 661, 10.1002/ana.1254 · DOI · Paper page
- Chang, 2005, Pathophysiological roles of amyloidogenic carboxy-terminal fragments of the beta-amyloid precursor protein in Alzheimer’s disease, J. Pharmacol. Sci., 97, 461, 10.1254/jphs.CR0050014 · DOI
- Chen, 2010, ApoE4 reduces glutamate receptor function and synaptic plasticity by selectively impairing ApoE receptor recycling, Proc. Natl. Acad. Sci. USA, 107, 12011, 10.1073/pnas.0914984107 · DOI · Paper page
- Coen, 2012, Lysosomal calcium homeostasis defects, not proton pump defects, cause endo-lysosomal dysfunction in PSEN-deficient cells, J. Cell Biol., 198, 23, 10.1083/jcb.201201076 · DOI · Paper page
- Dumanchin, 1999, Presenilins interact with Rab11, a small GTPase involved in the regulation of vesicular transport, Hum. Mol. Genet., 8, 1263, 10.1093/hmg/8.7.1263 · DOI · Paper page
- Fonseca, 2010, Cholesterol and statins in Alzheimer’s disease: current controversies, Exp. Neurol., 223, 282, 10.1016/j.expneurol.2009.09.013 · DOI · Paper page
- Gandy, 2007, Alzheimer’s presenilin 1 modulates sorting of APP and its carboxyl-terminal fragments in cerebral neurons in vivo, J. Neurochem., 102, 619, 10.1111/j.1471-4159.2007.04587.x · DOI
- Gatz, 2006, Role of genes and environments for explaining Alzheimer disease, Arch. Gen. Psychiatry, 63, 168, 10.1001/archpsyc.63.2.168 · DOI · Paper page
- Ginsberg, 2010, Microarray analysis of hippocampal CA1 neurons implicates early endosomal dysfunction during Alzheimer’s disease progression, Biol. Psychiatry, 68, 885, 10.1016/j.biopsych.2010.05.030 · DOI · Paper page
- Guo, 2012, Amyloid precursor protein revisited: neuron-specific expression and highly stable nature of soluble derivatives, J. Biol. Chem., 287, 2437, 10.1074/jbc.M111.315051 · DOI
- Karch, 2015, Alzheimer’s disease risk genes and mechanisms of disease pathogenesis, Biol. Psychiatry, 77, 43, 10.1016/j.biopsych.2014.05.006 · DOI · Paper page
- Kim, 2015, Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer’s disease, Mol. Psychiatry, 21, 1
- Kounnas, 1995, LDL receptor-related protein, a multifunctional ApoE receptor, binds secreted β-amyloid precursor protein and mediates its degradation, Cell, 82, 331, 10.1016/0092-8674(95)90320-8 · DOI · Paper page
- Lazo, 2013, BDNF regulates Rab11-mediated recycling endosome dynamics to induce dendritic branching, J. Neurosci., 33, 6112, 10.1523/JNEUROSCI.4630-12.2013 · DOI · Paper page
- Lee, 2010, Lysosomal proteolysis and autophagy require presenilin 1 and are disrupted by Alzheimer-related PS1 mutations, Cell, 141, 1146, 10.1016/j.cell.2010.05.008 · DOI · Paper page
- Lee, 2015, Presenilin 1 maintains lysosomal Ca2+ homeostasis via TRPML1 by regulating vATPase-mediated lysosome acidification, Cell Rep., 12, 1430, 10.1016/j.celrep.2015.07.050 · DOI · Paper page
- Leem, 2002, A role for presenilin 1 in regulating the delivery of amyloid precursor protein to the cell surface, Neurobiol. Dis., 11, 64, 10.1006/nbdi.2002.0546 · DOI
- Liu, 2013, Apolipoprotein E and Alzheimer disease: risk, mechanisms, and therapy, Nat. Rev, Neurol., 9, 106, 10.1038/nrneurol.2012.263 · DOI · Paper page
- Mauch, 2001, CNS synaptogenesis promoted by glia-derived cholesterol, Science, 294, 1354, 10.1126/science.294.5545.1354 · DOI · Paper page
- Maxfield, 2014, Role of endosomes and lysosomes in human disease, Cold Spring Harb. Perspect. Biol., 6, a016931, 10.1101/cshperspect.a016931 · DOI
- McBrayer, 2013, Lysosome and calcium dysregulation in Alzheimer’s disease: partners in crime, Biochem. Soc. Trans., 41, 1495, 10.1042/BST20130201 · DOI
- Nägler, 2001, Glia-derived signals induce synapse formation in neurones of the rat central nervous system, J. Physiol., 533, 665, 10.1111/j.1469-7793.2001.00665.x · DOI
- Neely, 2011, Presenilin is necessary for efficient proteolysis through the autophagy-lysosome system in a γ-secretase-independent manner, J. Neurosci., 31, 2781, 10.1523/JNEUROSCI.5156-10.2010 · DOI · Paper page
- Niederst, 2015, Axonal amyloid precursor protein and its fragments undergo somatodendritic endocytosis and processing, Mol. Biol. Cell, 26, 205, 10.1091/mbc.E14-06-1049 · DOI · Paper page
- Nixon, 2011, Autophagy failure in Alzheimer’s disease--locating the primary defect, Neurobiol. Dis., 43, 38, 10.1016/j.nbd.2011.01.021 · DOI · Paper page
- Peric, 2015, Early etiology of Alzheimer’s disease: tipping the balance toward autophagy or endosomal dysfunction?, Acta Neuropathol., 129, 363, 10.1007/s00401-014-1379-7 · DOI
- Pfrieger, 2003, Role of cholesterol in synapse formation and function. Biochim, Biophys. Acta, 1610, 271, 10.1016/S0005-2736(03)00024-5 · DOI · Paper page
- Pierrot, 2013, Amyloid precursor protein controls cholesterol turnover needed for neuronal activity, EMBO Mol. Med., 5, 608, 10.1002/emmm.201202215 · DOI
- Sakane, 2010, LRP6 is internalized by Dkk1 to suppress its phosphorylation in the lipid raft and is recycled for reuse, J. Cell Sci., 123, 360, 10.1242/jcs.058008 · DOI
- Selfridge, 2015, Rat embryonic hippocampus and induced pluripotent stem cell derived cultured neurons recover from laser-induced subaxotomy, Neurophotonics, 2, 015006, 10.1117/1.NPh.2.1.015006 · DOI
- Sinha, 1999, Cellular mechanisms of beta-amyloid production and secretion, Proc. Natl. Acad. Sci. USA, 96, 11049, 10.1073/pnas.96.20.11049 · DOI
- Spires-Jones, 2014, The intersection of amyloid beta and tau at synapses in Alzheimer’s disease, Neuron, 82, 756, 10.1016/j.neuron.2014.05.004 · DOI · Paper page
- Svennerholm, 1994, Membrane lipids, selectively diminished in Alzheimer brains, suggest synapse loss as a primary event in early-onset form (type I) and demyelination in late-onset form (type II), J. Neurochem., 62, 1039, 10.1046/j.1471-4159.1994.62031039.x · DOI
- Szpankowski, 2012, Subpixel colocalization reveals amyloid precursor protein-dependent kinesin-1 and dynein association with axonal vesicles, Proc. Natl. Acad. Sci. USA, 109, 8582, 10.1073/pnas.1120510109 · DOI
- Takahashi, 2007, Cholesterol controls lipid endocytosis through Rab11, Mol. Biol. Cell, 18, 2667, 10.1091/mbc.e06-10-0924 · DOI
- Tamboli, 2008, Loss of gamma-secretase function impairs endocytosis of lipoprotein particles and membrane cholesterol homeostasis, J. Neurosci., 28, 12097, 10.1523/JNEUROSCI.2635-08.2008 · DOI · Paper page
- Taylor, 2005, A microfluidic culture platform for CNS axonal injury, regeneration and transport, Nat. Methods, 2, 599, 10.1038/nmeth777 · DOI
- Toyn, 2014, Interpreting Alzheimer’s disease clinical trials in light of the effects on amyloid-β, Alzheimers Res. Ther., 6, 14, 10.1186/alzrt244 · DOI
- Udayar, 2013, A paired RNAi and RabGAP overexpression screen identifies Rab11 as a regulator of β-amyloid production, Cell Rep., 5, 1536, 10.1016/j.celrep.2013.12.005 · DOI · Paper page
- Ullrich, 1996, Rab11 regulates recycling through the pericentriolar recycling endosome, J. Cell Biol., 135, 913, 10.1083/jcb.135.4.913 · DOI · Paper page
- von Bartheld, 2004, Axonal transport and neuronal transcytosis of trophic factors, tracers, and pathogens, J. Neurobiol., 58, 295, 10.1002/neu.10315 · DOI
- Weissmiller, 2015, A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP, PLoS ONE, 10, e0118379, 10.1371/journal.pone.0118379 · DOI
- Welz, 2014, Orchestration of cell surface proteins by Rab11, Trends Cell Biol., 24, 407, 10.1016/j.tcb.2014.02.004 · DOI
- Wilson, 2000, EEA1, a tethering protein of the early sorting endosome, shows a polarized distribution in hippocampal neurons, epithelial cells, and fibroblasts, Mol. Biol. Cell, 11, 2657, 10.1091/mbc.11.8.2657 · DOI
- Wolozin, 2004, Cholesterol and the biology of Alzheimer’s disease, Neuron, 41, 7, 10.1016/S0896-6273(03)00840-7 · DOI · Paper page
- Woodruff, 2013, The presenilin-1 ΔE9 mutation results in reduced γ-secretase activity, but not total loss of PS1 function, in isogenic human stem cells, Cell Rep., 5, 974, 10.1016/j.celrep.2013.10.018 · DOI · Paper page
- Yamakawa, 2010, β-Secretase inhibitor potency is decreased by aberrant β-cleavage location of the “Swedish Mutant” amyloid precursor protein, J Biol Chem., 285, 1634, 10.1074/jbc.M109.066753 · DOI
- Yap, 2008, The somatodendritic endosomal regulator NEEP21 facilitates axonal targeting of L1/NgCAM, J. Cell Biol., 180, 827, 10.1083/jcb.200707143 · DOI
- Zhang, 2006, Presenilin/gamma-secretase activity regulates protein clearance from the endocytic recycling compartment, FASEB J., 20, 1176, 10.1096/fj.05-5531fje · DOI
Cited by
Sorted by citations
Amyloid-β-independent regulators of tau pathology in Alzheimer disease
van der Kant, R., Goldstein, L. S. B., & Ossenkoppele, R. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-019-0240-3 · Cited by 580
Self-citationNixon, R. A. (2017) · The FASEB Journal · doi:10.1096/fj.201700359 · Cited by 400
Hung, C. O. Y., & Livesey, F. J. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.11.095 · Cited by 159
Im, E., Jiang, Y., Stavrides, P. H., Darji, S., Erdjument-Bromage, H., Neubert, T. A., Choi, J. Y., Wegiel, J., Lee, J.-H., & Nixon, R. A. (2023) · Science Advances · doi:10.1126/sciadv.adg1925 · Cited by 80
Human iPSC application in Alzheimer’s disease and tau-related neurodegenerative diseases
TCW, J. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.01.043 · Cited by 39
Aging impact on amyloid precursor protein neuronal trafficking
Burrinha, T., & Guimas Almeida, C. (2022) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2022.102524 · Cited by 26
Pilat, D., Paumier, J.-M., García-González, L., Louis, L., Stephan, D., Manrique, C., Khrestchatisky, M., Di Pasquale, E., Baranger, K., & Rivera, S. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02407-z · Cited by 28
Metadata
- Authors
- Woodruff, G., Reyna, S. M., Dunlap, M., Van Der Kant, R., Callender, J. A., Young, J. E., Roberts, E. A., & Goldstein, L. S. B.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 17
- Issue
- 3
- Pages
- 759-773
- ISSN
- 2211-1247
- PMC
- PMC5796664
- Cited by
- 105
- References
- 10
- 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