The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Partial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF
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?
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“VPS35 dysfunction leads to APP accumulation in early endosomes, increased Aβ production and exosomal release, and enlarged axonal endosomes [9, 16, 20].”
From Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer’s disease mouse model (2025) · cites this paper as [16]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“VPS35 dysfunction leads to APP accumulation in early endosomes, increased Aβ production and exosomal release, and enlarged axonal endosomes [9, 16, 20].”
From Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer’s disease mouse model (2025) · cites this paper as [16]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“VPS35 dysfunction leads to APP accumulation in early endosomes, increased Aβ production and exosomal release, and enlarged axonal endosomes [9, 16, 20].”
From Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer’s disease mouse model (2025) · cites this paper as [16]
Experimental — accuracy not yet measured
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
West, M. J., Slomianka, L., & Gundersen, H. J. G. (1991) · The Anatomical Record · doi:10.1002/ar.1092310411 · Cited by 2,994 · cited 1×
“The numbers of ChAT-immunoreactive BFCNs in the medial septal nucleus (MSN) were determined using the optical fractionator method (West et al., 1991) using ImageJ software as previously described (Smiley et al., 2012).”
Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921
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
Cataldo, A. M., Barnett, J. L., Pieroni, C., & Nixon, R. A. (1997) · The Journal of Neuroscience · doi:10.1523/jneurosci.17-16-06142.1997 · Cited by 393
Self-citationMcConlogue, L., Buttini, M., Anderson, J. P., Brigham, E. F., Chen, K. S., Freedman, S. B., Games, D., Johnson-Wood, K., Lee, M., Zeller, M., et al. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m611687200 · Cited by 300 · cited 5×
“reducing APP-bCTF while minimally changing Ab levels, as previously reported (McConlogue et al., 2007; Nishitomi et al., 2006), to investigate its possible therapeutic effects.”
InfluentialCataldo, A. M., Petanceska, S., Peterhoff, C. M., Terio, N. B., Epstein, C. J., Villar, A., Carlson, E. J., Staufenbiel, M., & Nixon, R. A. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-17-06788.2003 · Cited by 241 · cited 8×
“4G and H) in Ts2 mice at 4 months of age, and the enlargement is comparable to that seen in age-matched Ts65Dn mice (Cataldo et al., 2003).”
InfluentialSelf-citationLauritzen, I., Pardossi-Piquard, R., Bauer, C., Brigham, E., Abraham, J.-D., Ranaldi, S., Fraser, P., St-George-Hyslop, P., Le Thuc, O., Espin, V., et al. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.2775-12.2012 · Cited by 201 · cited 1×
“The present results add to a growing body of evidence that, independently of its conversion to Ab, APP-bCTF has neurotoxic properties that are pathogenic in AD (Devi and Ohno, 2011; Lauritzen et al., 2012; Kim et al., 2015; McPhie et al., 2001; Tamayev et al., 2012).”
Research works printed but not linked: 48
- Barman, 2014, Computational insights into substrate and site specificities, catalytic mechanism, and protonation states of the catalytic asp dyad of beta -Secretase, Scientifica (Cairo), 2014, 598728
- Cai, 2001, BACE1 is the major beta-secretase for generation of Abeta peptides by neurons, Nat. Neurosci., 4, 233, 10.1038/85064 · DOI
- Cataldo, 2008, Down syndrome fibroblast model of Alzheimer-related endosome pathology. Accelerated endocytosis promotes late endocytic defects, Am. J. Pathol., 173, 370, 10.2353/ajpath.2008.071053 · DOI
- Cataldo, 2000, Endocytic pathway abnormalities precede amyloid beta 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
- Chen, 2009, In vivo MRI identifies cholinergic circuitry deficits in a Down syndrome model, Neurobiol. Aging, 30, 1453, 10.1016/j.neurobiolaging.2007.11.026 · DOI
- Choi, 2009, Age-dependent dysregulation of brain APP in the Ts65Dn Down syndrome mouse model, J. Neurochem., 110, 1818, 10.1111/j.1471-4159.2009.06277.x · DOI · Paper page
- Choi, 2013, Early endosomal abnormalities and cholinergic neuron degeneration in amyloid-beta protein precursor transgenic mice, J. Alzheimers Dis., 34, 691, 10.3233/JAD-122143 · DOI
- Cossec, 2012, Trisomy for synaptojanin1 in Down syndrome is functionally linked to the enlargement of early endosomes, Hum. Mol. Genet., 21, 3156, 10.1093/hmg/dds142 · DOI
- Davisson, 1990, Segmental trisomy of murine chromosome 16: a new model system for studying Down syndrome, Prog. Clin. Biol. Res., 360, 263
- Davisson, 1993, Segmental trisomy as a mouse model for Down syndrome, Prog. Clin. Biol. Res., 384, 117
- Deinhardt, 2006, Rab5 and Rab7 control endocytic sorting along the axonal retrograde transport pathway, Neuron, 52, 293, 10.1016/j.neuron.2006.08.018 · DOI
- Devi, 2011, Mitochondrial dysfunction and accumulation of the beta-secretase-cleaved C-terminal fragment of APP in Alzheimer's disease transgenic mice, Neurobiol. Dis., 45, 417, 10.1016/j.nbd.2011.09.001 · DOI
- Gouras, 1998, Generation and regulation of beta-amyloid peptide variants by neurons, J. Neurochem., 71, 1920, 10.1046/j.1471-4159.1998.71051920.x · DOI
- Granholm, 2000, Loss of cholinergic phenotype in basal forebrain coincides with cognitive decline in a mouse model of Down's syndrome, Exp. Neurol., 161, 647, 10.1006/exnr.1999.7289 · DOI
- Holtzman, 1996, Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome, Proc. Natl. Acad. Sci. U. S. A., 93, 13333, 10.1073/pnas.93.23.13333 · DOI · Paper page
- Hunter, 2004, Minocycline prevents cholinergic loss in a mouse model of Down's syndrome, Ann. Neurol., 56, 675, 10.1002/ana.20250 · DOI
- Imbimbo, 2008, Therapeutic potential of gamma-secretase inhibitors and modulators, Curr. Top. Med. Chem., 8, 54, 10.2174/156802608783334015 · DOI · Paper page
- Jiang, 2010, Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition, Proc. Natl. Acad. Sci. U. S. A., 107, 1630, 10.1073/pnas.0908953107 · DOI
- Kaether, 2006, Amyloid precursor protein and Notch intracellular domains are generated after transport of their precursors to the cell surface, Traffic, 7, 408, 10.1111/j.1600-0854.2006.00396.x · DOI
- Kaur, 2014, Glutamatergic transmission aberration: a major cause of behavioral deficits in a murine model of Down's syndrome, J. Neurosci., 34, 5099, 10.1523/JNEUROSCI.5338-13.2014 · 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
- Kobayashi, 2008, BACE1 gene deletion: impact on behavioral function in a model of Alzheimer's disease, Neurobiol. Aging, 29, 861, 10.1016/j.neurobiolaging.2007.01.002 · DOI · Paper page
- Laifenfeld, 2007, Rab5 mediates an amyloid precursor protein signaling pathway that leads to apoptosis, J. Neurosci., 27, 7141, 10.1523/JNEUROSCI.4599-06.2007 · DOI
- Laird, 2005, BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions, J. Neurosci., 25, 11693, 10.1523/JNEUROSCI.2766-05.2005 · DOI · Paper page
- Lee, 2005, BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivo, J. Cell Biol., 168, 291, 10.1083/jcb.200407070 · DOI · Paper page
- Lockrow, 2009, Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model, Exp. Neurol., 216, 278, 10.1016/j.expneurol.2008.11.021 · DOI
- Luo, 2003, Biochemical and genetic evidence for the involvement of yeast Ypt6-GTPase in protein retrieval to different Golgi compartments, J. Biol. Chem., 278, 791, 10.1074/jbc.M209120200 · DOI
- McPhie, 2001, beta-Secretase cleavage of the amyloid precursor protein mediates neuronal apoptosis caused by familial Alzheimer's disease mutations, Brain Res. Mol. Brain Res., 97, 103, 10.1016/S0169-328X(01)00294-7 · DOI
- Moore, 2010, Increased male reproductive success in Ts65Dn “Down syndrome” mice, Mamm. Genome, 21, 543, 10.1007/s00335-010-9300-8 · DOI
- Moore, 2015, APP metabolism regulates tau proteostasis in human cerebral cortex neurons, Cell Rep., 11, 689, 10.1016/j.celrep.2015.03.068 · DOI · Paper page
- Nishitomi, 2006, BACE1 inhibition reduces endogenous Abeta and alters APP processing in wild-type mice, J. Neurochem., 99, 1555, 10.1111/j.1471-4159.2006.04178.x · DOI
- Nixon, 2013, The role of autophagy in neurodegenerative disease, Nat. Med., 19, 983, 10.1038/nm.3232 · DOI · Paper page
- Ohno, 2007, BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice, Neurobiol. Dis., 26, 134, 10.1016/j.nbd.2006.12.008 · DOI · Paper page
- Pastorino, 2004, BACE (beta-secretase) modulates the processing of APLP2 in vivo, Mol. Cell. Neurosci., 25, 642, 10.1016/j.mcn.2003.12.013 · DOI
- Pera, 2013, Distinct patterns of APP processing in the CNS in autosomal-dominant and sporadic Alzheimer disease, Acta Neuropathol., 125, 201, 10.1007/s00401-012-1062-9 · DOI · Paper page
- Salehi, 2006, Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration, Neuron, 51, 29, 10.1016/j.neuron.2006.05.022 · DOI · Paper page
- Schmidt, 2005, Tissue processing prior to protein analysis and amyloid-beta quantitation, Methods Mol. Biol., 299, 267
- Schmidt, 2005, ELISA method for measurement of amyloid-beta levels, Methods Mol. Biol., 299, 279
- Seo, 2005, Abnormal APP, cholinergic and cognitive function in Ts65Dn Down's model mice, Exp. Neurol., 193, 469, 10.1016/j.expneurol.2004.11.017 · DOI
- Singer, 2005, Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model, Nat. Neurosci., 8, 1343, 10.1038/nn1531 · DOI
- Sinha, 1999, Purification and cloning of amyloid precursor protein beta-secretase from human brain, Nature, 402, 537, 10.1038/990114 · DOI · Paper page
- Smiley, 2012, Cortical thickness, neuron density and size in the inferior parietal lobe in schizophrenia, Schizophr. Res., 136, 43, 10.1016/j.schres.2012.01.006 · DOI
- Tamayev, 2012, Inhibition of gamma-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia, Mol. Neurodegener., 7, 19, 10.1186/1750-1326-7-19 · DOI · Paper page
- Tamayev, 2012, beta- but not gamma-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia, EMBO Mol. Med., 4, 171, 10.1002/emmm.201100195 · DOI · Paper page
- Tomasselli, 2003, Employing a superior BACE1 cleavage sequence to probe cellular APP processing, J. Neurochem., 84, 1006, 10.1046/j.1471-4159.2003.01597.x · DOI
- Villar, 2005, Identification and characterization of a new Down syndrome model, Ts[Rb(12.1716)]2Cje, resulting from a spontaneous Robertsonian fusion between T(171)65Dn and mouse chromosome 12, Mamm. Genome, 16, 79, 10.1007/s00335-004-2428-7 · DOI
- Walter, 2001, Phosphorylation regulates intracellular trafficking of beta-secretase, J. Biol. Chem., 276, 14634, 10.1074/jbc.M011116200 · DOI · Paper page
- Weissmiller, 2015, A gamma-secretase inhibitor, but not a gamma-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
Cited by
Sorted by citations
Mechanisms of autophagy–lysosome dysfunction in neurodegenerative diseases
Nixon, R. A., & Rubinsztein, D. C. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00757-5 · Cited by 435
Self-citationLysosomal Dysfunction in Down Syndrome Is APP-Dependent and Mediated by APP-βCTF (C99)
Jiang, Y., Sato, Y., Im, E., Berg, M., Bordi, M., Darji, S., Kumar, A., Mohan, P. S., Bandyopadhyay, U., Diaz, A., et al. (2019) · The Journal of Neuroscience · doi:10.1523/jneurosci.0578-19.2019 · Cited by 166
Self-citationHung, C. O. Y., & Livesey, F. J. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.11.095 · Cited by 159
The endosomal-lysosomal pathway is dysregulated by APOE4 expression in vivo
Nuriel, T., Peng, K. Y., Ashok, A., Dillman, A. A., Figueroa, H. Y., Apuzzo, J., Ambat, J., Levy, E., Cookson, M. R., Mathews, P. M., et al. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00702 · Cited by 140
Self-citationIm, 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
Self-citation
Metadata
- Authors
- Jiang, Y., Rigoglioso, A., Peterhoff, C. M., Pawlik, M., Sato, Y., Bleiwas, C., Stavrides, P., Smiley, J. F., Ginsberg, S. D., Mathews, P. M., Levy, E., & Nixon, R. A.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2016-03
- Volume
- 39
- Pages
- 90-98
- ISSN
- 0197-4580
- PMC
- PMC4773919
- Cited by
- 97
- References
- 7
- Language
- en
- Funders
- National Institutes of Health
- National Institute on Aging (P01AG017617, AG043375)
- Alzheimer's Association (IIRG-12-237253, IIRG-07-60047)
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