The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Endolysosome involvement in LDL cholesterol-induced Alzheimer's disease-like pathology in primary cultured neurons
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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.”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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.”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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.”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
Experimental — accuracy not yet measuredIn the citing paper
“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.”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
In the citing paper
“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.”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
In the citing paper
“For this reason, the LDL concentration adopted in our study followed methodological precedent established by previous investigations examining LDL effects on CNS cells (Hui et al. 2012; Moreira et al. 2012; Engel et al. 2016, 2019; Farias et al. 2025).”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Hui et al. 2012
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
Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Rimmler, J. B., Locke, P. A., Conneally, P. M., Schmader, K. E., et al. (1994) · Nature Genetics · doi:10.1038/ng0694-180 · Cited by 1,920
Genetic associations with human longevity at the APOE and ACE loci
Schächter, F., Faure-Delanef, L., Guénot, F., Rouger, H., Froguel, P., Lesueur-Ginot, L., & Cohen, D. (1994) · Nature Genetics · doi:10.1038/ng0194-29 · Cited by 1,095
Tau fragmentation, aggregation and clearance: the dual role of lysosomal processing
Wang, Y., Martinez-Vicente, M., Krüger, U., Kaushik, S., Wong, E., Mandelkow, E.-M., Cuervo, A. M., & Mandelkow, E. (2009) · Human Molecular Genetics · doi:10.1093/hmg/ddp367 · Cited by 617 · cited 2×
“Tau is degraded by cathepsin D in autophagosomes–lysosomes (Hamano et al., 2008; Kenessey et al., 1997; Oyama et al., 1998; Wang et al., 2009), and increased levels of cholesterol in lysosomes cause lysosome dysfunction and tau-pathology in brains of patients with Niemann-Pick type C disease (Bi and Liao, 2007; Bu et…”
Solomon, A., Kivipelto, M., Wolozin, B., Zhou, J., & Whitmer, R. A. (2009) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000231980 · Cited by 557
Association of γ-Secretase with Lipid Rafts in Post-Golgi and Endosome Membranes
Vetrivel, K. S., Cheng, H., Lin, W., Sakurai, T., Li, T., Nukina, N., Wong, P. C., Xu, H., & Thinakaran, G. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m407986200 · Cited by 413
Blood—Brain Barrier Permeability Precedes Senile Plaque Formation in an Alzheimer Disease Model
UJIIE, M., DICKSTEIN, D. L., CARLOW, D. A., & JEFFERIES, W. A. (2003) · Microcirculation · doi:10.1038/sj.mn.7800212 · Cited by 351
Liao, G., Yao, Y., Liu, J., Yu, Z., Cheung, S., Xie, A., Liang, X., & Bi, X. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.070052 · Cited by 220
Caffeine protects against MPTP‐induced blood‐brain barrier dysfunction in mouse striatum
Chen, X., Lan, X., Roche, I., Liu, R., & Geiger, J. D. (2008) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2008.05697.x · Cited by 189
Self-citationEffects of cellular cholesterol loading on macrophage foam cell lysosome acidification
Cox, B. E., Griffin, E. E., Ullery, J. C., & W. Gray, J. (2007) · Journal of Lipid Research · doi:10.1194/jlr.m600390-jlr200 · Cited by 110
Research works printed but not linked: 76
- Arriagada, 2007, Endosomal abnormalities related to amyloid precursor protein in cholesterol treated cerebral cortex neuronal cells derived from trisomy 16 mice, an animal model of Down syndrome, Neurosci Lett, 423, 172, 10.1016/j.neulet.2007.06.054 · DOI
- Bahr, 2002, The neuropathogenic contributions of lysosomal dysfunction, J Neurochem, 83, 481, 10.1046/j.1471-4159.2002.01192.x · DOI
- Bendiske, 2003, Lysosomal activation is a compensatory response against protein accumulation and associated synaptopathogenesis—an approach for slowing Alzheimer disease?, J Neuropathol Exp Neurol, 62, 451, 10.1093/jnen/62.5.451 · DOI
- Bendiske, 2002, Intracellular deposition, microtubule destabilization, and transport failure: an “early” pathogenic cascade leading to synaptic decline, J Neuropathol Exp Neurol, 61, 640, 10.1093/jnen/61.7.640 · DOI
- Bi, 2007, Autophagic-lysosomal dysfunction and neurodegeneration in Niemann-Pick type C mice: lipid starvation or indigestion?, Autophagy, 3, 646, 10.4161/auto.5074 · DOI
- Blennow, 2006, Alzheimer's disease, Lancet, 368, 387, 10.1016/S0140-6736(06)69113-7 · DOI · Paper page
- Blumstein, 2001, The neuronal form of adaptor protein-3 is required for synaptic vesicle formation from endosomes, J Neurosci, 21, 8034, 10.1523/JNEUROSCI.21-20-08034.2001 · DOI · Paper page
- Boland, 2008, Autophagy induction and autophagosome clearance in neurons: relationship to autophagic pathology in Alzheimer's disease, J Neurosci, 28, 6926, 10.1523/JNEUROSCI.0800-08.2008 · DOI · Paper page
- Bu, 2002, Deregulation of cdk5, hyperphosphorylation, and cytoskeletal pathology in the Niemann-Pick type C murine model, J Neurosci, 22, 6515, 10.1523/JNEUROSCI.22-15-06515.2002 · DOI
- Callahan, 1999, Quantitative decrease in synaptophysin message expression and increase in cathepsin D message expression in Alzheimer disease neurons containing neurofibrillary tangles, J Neuropathol Exp Neurol, 58, 275, 10.1097/00005072-199903000-00007 · DOI
- Castellani, 2010, Alzheimer disease, Dis Mon, 56, 484, 10.1016/j.disamonth.2010.06.001 · DOI
- Cataldo, 1990, Lysosomal proteinase antigens are prominently localized within senile plaques of Alzheimer's disease: evidence for a neuronal origin, Brain Res, 513, 181, 10.1016/0006-8993(90)90456-L · DOI
- Cataldo, 1994, Lysosomal abnormalities in degenerating neurons link neuronal compromise to senile plaque development in Alzheimer disease, Brain Res, 640, 68, 10.1016/0006-8993(94)91858-9 · DOI · Paper page
- 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
- Cataldo, 2004, Abeta localization in abnormal endosomes: association with earliest Abeta elevations in AD and Down syndrome, Neurobiol Aging, 25, 1263, 10.1016/j.neurobiolaging.2004.02.027 · DOI · Paper page
- Chen, 2008, Caffeine blocks disruption of blood brain barrier in a rabbit model of Alzheimer's disease, J Neuroinflammation, 5, 12, 10.1186/1742-2094-5-12 · DOI
- Chen, 2010, Endolysosome mechanisms associated with Alzheimer's disease-like pathology in rabbits ingesting cholesterol-enriched diet, J Alzheimers Dis, 22, 1289, 10.3233/JAD-2010-101323 · DOI
- Chyung, 2003, Inhibition of receptor-mediated endocytosis demonstrates generation of amyloid beta-protein at the cell surface, J Biol Chem, 278, 51035, 10.1074/jbc.M304989200 · DOI · Paper page
- Corder, 1993, Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families, Science, 261, 921, 10.1126/science.8346443 · DOI · Paper page
- Corder, 1996, Apolipoprotein E genotype and the rate of decline in probable Alzheimer disease, Arch Neurol, 53, 1094, 10.1001/archneur.1996.00550110022004 · DOI
- Cossec, 2010, Cholesterol changes in Alzheimer's disease: methods of analysis and impact on the formation of enlarged endosomes, Biochim Biophys Acta, 1801, 839, 10.1016/j.bbalip.2010.03.010 · DOI
- Crisby, 2004, Effects of high cholesterol diet on gliosis in apolipoprotein E knockout mice. Implications for Alzheimer's disease and stroke, Neurosci Lett, 369, 87, 10.1016/j.neulet.2004.05.057 · DOI
- Dallongeville, 1992, Modulation of plasma triglyceride levels by apoE phenotype: a meta-analysis, J Lipid Res, 33, 447, 10.1016/S0022-2275(20)41611-6 · DOI
- Distl, 2003, Cholesterol storage and tau pathology in Niemann-Pick type C disease in the brain, J Pathol, 200, 104, 10.1002/path.1320 · DOI
- Ferreira, 1993, Intraneuronal compartments of the amyloid precursor protein, J Neurosci, 13, 3112, 10.1523/JNEUROSCI.13-07-03112.1993 · DOI
- Frykman, 2010, Synaptic and endosomal localization of active gamma-secretase in rat brain, PLoS One, 5, e8948, 10.1371/journal.pone.0008948 · DOI · Paper page
- Ghribi, 2006, High cholesterol content in neurons increases BACE, beta-amyloid, and phosphorylated tau levels in rabbit hippocampus, Exp Neurol, 200, 460, 10.1016/j.expneurol.2006.03.019 · DOI · Paper page
- Granholm, 2008, Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat, J Alzheimers Dis, 14, 133, 10.3233/JAD-2008-14202 · DOI
- Hamano, 2008, Autophagic-lysosomal perturbation enhances tau aggregation in transfectants with induced wild-type tau expression, Eur J Neurosci, 27, 1119, 10.1111/j.1460-9568.2008.06084.x · DOI · Paper page
- Hamazaki, 1996, Cathepsin D is involved in the clearance of Alzheimer's beta-amyloid protein, FEBS Lett, 396, 139, 10.1016/0014-5793(96)01087-3 · DOI · Paper page
- Hardy, 2009, The amyloid hypothesis for Alzheimer's disease: a critical reappraisal, J Neurochem, 110, 1129, 10.1111/j.1471-4159.2009.06181.x · DOI · Paper page
- Harris, 2010, Cholesterol in Alzheimer's disease and other amyloidogenic disorders, Subcell Biochem, 51, 47, 10.1007/978-90-481-8622-8_2 · DOI · Paper page
- He, 2007, Degradation of nicastrin involves both proteasome and lysosome, J Neurochem, 101, 982, 10.1111/j.1471-4159.2007.04449.x · DOI
- Higaki, 1996, Processing of beta-amyloid precursor protein by cathepsin D, J Biol Chem, 271, 31885, 10.1074/jbc.271.50.31885 · DOI
- Kalaria, 1999, The blood–brain barrier and cerebrovascular pathology in Alzheimer's disease, Ann N Y Acad Sci, 893, 113, 10.1111/j.1749-6632.1999.tb07821.x · DOI
- Kanju, 2007, Lysosomal dysfunction produces distinct alterations in synaptic alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid and N-methyl-d-aspartate receptor currents in hippocampus, J Neuropathol Exp Neurol, 66, 779, 10.1097/nen.0b013e3181461ae7 · DOI
- Kenessey, 1997, Degradation of tau by lysosomal enzyme cathepsin D: implication for Alzheimer neurofibrillary degeneration, J Neurochem, 69, 2026, 10.1046/j.1471-4159.1997.69052026.x · DOI
- Koh, 2005, BACE is degraded via the lysosomal pathway, J Biol Chem, 280, 32499, 10.1074/jbc.M506199200 · DOI
- Kuromi, 1998, Two distinct pools of synaptic vesicles in single presynaptic boutons in a temperature-sensitive Drosophila mutant, shibire, Neuron, 20, 917, 10.1016/S0896-6273(00)80473-0 · DOI
- Ladror, 1994, Cleavage at the amino and carboxyl termini of Alzheimer's amyloid-beta by cathepsin D, J Biol Chem, 269, 18422, 10.1016/S0021-9258(17)32325-6 · DOI
- Marzolo, 2009, Lipoprotein receptors and cholesterol in APP trafficking and proteolytic processing, implications for Alzheimer's disease, Semin Cell Dev Biol, 20, 191, 10.1016/j.semcdb.2008.10.005 · DOI · Paper page
- Maxfield, 2005, Role of cholesterol and lipid organization in disease, Nature, 438, 612, 10.1038/nature04399 · DOI
- Murthy, 1998, Synaptic vesicles retain their identity through the endocytic cycle, Nature, 392, 497, 10.1038/33152 · DOI
- Namba, 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, 10.1016/0304-3940(92)90531-B · DOI
- Nieweg, 2009, Marked differences in cholesterol synthesis between neurons and glial cells from postnatal rats, J Neurochem, 109, 125, 10.1111/j.1471-4159.2009.05917.x · DOI · Paper page
- Nixon, 2005, Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases, Neurobiol Aging, 26, 373, 10.1016/j.neurobiolaging.2004.09.018 · DOI
- Nixon, 2007, Autophagy, amyloidogenesis and Alzheimer disease, J Cell Sci, 120, 4081, 10.1242/jcs.019265 · DOI · Paper page
- Oyama, 1998, Chloroquine myopathy suggests that tau is degraded in lysosomes: implication for the formation of paired helical filaments in Alzheimer's disease, Neurosci Res, 31, 1, 10.1016/S0168-0102(98)00020-0 · DOI
- Pasternak, 2003, Presenilin-1, nicastrin, amyloid precursor protein, and gamma-secretase activity are co-localized in the lysosomal membrane, J Biol Chem, 278, 26687, 10.1074/jbc.M304009200 · DOI
- Pasternak, 2004, The role of the endosomal/lysosomal system in amyloid-beta production and the pathophysiology of Alzheimer's disease: reexamining the spatial paradox from a lysosomal perspective, J Alzheimers Dis, 6, 53, 10.3233/JAD-2004-6107 · DOI
- Perez, 1999, Mutagenesis identifies new signals for beta-amyloid precursor protein endocytosis, turnover, and the generation of secreted fragments, including Abeta42, J Biol Chem, 274, 18851, 10.1074/jbc.274.27.18851 · DOI
- Pitas, 1987, Lipoproteins and their receptors in the central nervous system. Characterization of the lipoproteins in cerebrospinal fluid and identification of apolipoprotein B, E(LDL) receptors in the brain, J Biol Chem, 262, 14352, 10.1016/S0021-9258(18)47945-8 · DOI · Paper page
- Rajendran, 2008, Efficient inhibition of the Alzheimer's disease beta-secretase by membrane targeting, Science, 320, 520, 10.1126/science.1156609 · DOI
- Refolo, 1995, Evidence that secretase cleavage of cell surface Alzheimer amyloid precursor occurs after normal endocytic internalization, J Neurosci Res, 40, 694, 10.1002/jnr.490400515 · DOI
- Reiss, 2004, Cholesterol in neurologic disorders of the elderly: stroke and Alzheimer's disease, Neurobiol Aging, 25, 977, 10.1016/j.neurobiolaging.2003.11.009 · DOI · Paper page
- Saftig, 1996, Amyloidogenic processing of human amyloid precursor protein in hippocampal neurons devoid of cathepsin D, J Biol Chem, 271, 27241, 10.1074/jbc.271.44.27241 · DOI
- Sawamura, 2001, Site-specific phosphorylation of tau accompanied by activation of mitogen-activated protein kinase (MAPK) in brains of Niemann-Pick type C mice, J Biol Chem, 276, 10314, 10.1074/jbc.M009733200 · DOI
- Scuteri, 2001, Is the apoE4 allele an independent predictor of coronary events?, Am J Med, 110, 28, 10.1016/S0002-9343(00)00639-2 · DOI
- Seabrook, 2007, Beyond amyloid: the next generation of Alzheimer's disease therapeutics, Mol Interv, 7, 261, 10.1124/mi.7.5.8 · DOI
- Selkoe, 2002, Alzheimer's disease is a synaptic failure, Science, 298, 789, 10.1126/science.1074069 · DOI · Paper page
- Shimizu, 2008, Crystal structure of an active form of BACE1, an enzyme responsible for amyloid beta protein production, Mol Cell Biol, 28, 3663, 10.1128/MCB.02185-07 · DOI · Paper page
- Sleat, 2004, Genetic evidence for nonredundant functional cooperativity between NPC1 and NPC2 in lipid transport, Proc Natl Acad Sci U S A, 101, 5886, 10.1073/pnas.0308456101 · DOI
- Soriano, 1999, Expression of beta-amyloid precursor protein-CD3gamma chimeras to demonstrate the selective generation of amyloid beta(1–40) and amyloid beta(1–42) peptides within secretory and endocytic compartments, J Biol Chem, 274, 32295, 10.1074/jbc.274.45.32295 · DOI
- Sparks, 2008, The early and ongoing experience with the cholesterol-fed rabbit as a model of Alzheimer's disease: the old, the new and the pilot, J Alzheimers Dis, 15, 641, 10.3233/JAD-2008-15410 · DOI
- Sparks, 1994, Induction of Alzheimer-like beta-amyloid immunoreactivity in the brains of rabbits with dietary cholesterol, Exp Neurol, 126, 88, 10.1006/exnr.1994.1044 · DOI · Paper page
- Sparks, 2000, Link between heart disease, cholesterol, and Alzheimer's disease: a review, Microsc Res Tech, 50, 287, 10.1002/1097-0029(20000815)50:4<287::AID-JEMT7>3.0.CO;2-L · DOI
- Takechi, 2009, Three-dimensional colocalization analysis of plasma-derived apolipoprotein B with amyloid plaques in APP/PS1 transgenic mice, Histochem Cell Biol, 131, 661, 10.1007/s00418-009-0567-3 · DOI
- Tate, 2006, Targeting the role of the endosome in the pathophysiology of Alzheimer's disease: a strategy for treatment, Sci Aging Knowledge Environ, 10, re2
- Terry, 1991, Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment, Ann Neurol, 30, 572, 10.1002/ana.410300410 · DOI · Paper page
- Thirumangalakudi, 2008, High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice, J Neurochem, 106, 475, 10.1111/j.1471-4159.2008.05415.x · DOI · Paper page
- Vance, 2006, Lipid imbalance in the neurological disorder, Niemann-Pick C disease, FEBS Lett, 580, 5518, 10.1016/j.febslet.2006.06.008 · DOI
- Vance, 2006, Lipid dynamics in neurons, Biochem Soc Trans, 34, 399, 10.1042/BST0340399 · DOI
- Vassar, 1999, Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE, Science, 286, 735, 10.1126/science.286.5440.735 · DOI · Paper page
- Wisdom, 2011, The effects of apolipoprotein E on non-impaired cognitive functioning: a meta-analysis, Neurobiol Aging, 32, 63, 10.1016/j.neurobiolaging.2009.02.003 · DOI
- Yuyama, 2009, Late endocytic dysfunction as a putative cause of amyloid fibril formation in Alzheimer's disease, J Neurochem, 109, 1250, 10.1111/j.1471-4159.2009.06046.x · DOI
- Zipser, 2007, Microvascular injury and blood–brain barrier leakage in Alzheimer's disease, Neurobiol Aging, 28, 977, 10.1016/j.neurobiolaging.2006.05.016 · DOI · Paper page
Cited by
Sorted by citations
Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease
Cai, Z., Hussain, M. D., & Yan, L.-J. (2014) · International Journal of Neuroscience · doi:10.3109/00207454.2013.833510 · Cited by 583
Colacurcio, D. J., & Nixon, R. A. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.05.004 · Cited by 548
Cholesterol impairs autophagy-mediated clearance of amyloid beta while promoting its secretion
Barbero-Camps, E., Roca-Agujetas, V., Bartolessis, I., de Dios, C., Fernández-Checa, J. C., Marí, M., Morales, A., Hartmann, T., & Colell, A. (2018) · Autophagy · doi:10.1080/15548627.2018.1438807 · Cited by 125
Baumart, G. J., Rodrigues, M. S., Sholl, J. N., de Sousa, A. C., Weber, A. F., Costa‐Beber, L. C., Farias, H. R., Costa, M. V., Peres, A. M., de Camargo, P. R., et al. (2026) · Journal of Neurochemistry · doi:10.1111/jnc.70403 · Cited by 2
Metadata
- Authors
- Hui, L., Chen, X., & Geiger, J. D.
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 2012-12
- Volume
- 91
- Issue
- 23-24
- Pages
- 1159-1168
- ISSN
- 0024-3205
- PMC
- PMC3431446
- Cited by
- 58
- References
- 9
- Language
- en
- Funders
- National Center for Research Resources (P20RR17699)
- NIH
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
