CoChat
Sign Up
Cited by 58

The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

Cell-type-specific regulation of APOE and CLU levels in human neurons by the Alzheimer’s disease risk gene SORL1

Lee, Hyo, Aylward, Aimee J., Pearse, Richard V., Lish, Alexandra M., Hsieh, Yi-Chen, Augur, Zachary M., Benoit, Courtney R., Chou, Vicky, Knupp, Allison, Pan, Cheryl, Goberdhan, Srilakshmi, Duong, Duc M., Seyfried, Nicholas T., Bennett, David A., Taga, Mariko F., Huynh, Kevin, Arnold, Matthias, Meikle, Peter J., De Jager, Philip L., Menon, Vilas, Young, Jessica E., Young-Pearse, Tracy L.·2023·Cell Reports
DOI 10.1016/j.celrep.2023.112994PMC PMC10568487
Open this paper in CoChat — free account

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.celrep.2023.112994

Cites

14 of 14 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Depletion of SORLA in neurons leads to enlarged early endosomes, impairments in endo-lysosomal trafficking, changes in gene expression, and impaired neuronal function.

    “Recent work from our group and others has shown that depletion of SORLA in neurons leads to enlarged early endosomes, impairments in endo‐lysosomal trafficking, changes in gene expression, and impaired neuronal function (Hung et al. 2021; Knupp et al. 2020; Lee et al. 2023; Mishra et al. 2023, 2022).”

    From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Lee et al. 2023

    The Introduction reports impaired endosomal trafficking after SORL1 loss in iPSC-derived neurons, and the Results report enlarged early endosomes and altered gene expression. The Results also show increased Aβ and phosphorylated tau, but the passages do not establish impaired neuronal function as a consequence of SORL1 depletion. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • SORL1 is highly expressed in the central nervous system, including in microglia.

    “SORL1 is highly expressed in the central nervous system, including in microglia, the tissue‐resident immune cells of the brain.”

    From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Lee et al. 2023

  • Previous reports indicate that SORLA deletion in iPSC-derived astrocytes, neurons or microglia had little effect on retromer components.

    “Proteomics analyses from previous reports indicate that SORLA deletion in iPSC-derived astrocytes, neurons or microglia had little effect on retromer components (Lee, Aylward et al. 2023) (Figure S6B); similarly we find little difference in retromer components (VPS35, VPS26a) in WT compared to SORLA KO, PS19 or SORLA KO/PS19 brain (Figure S6C, D).”

    From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Lee, Aylward et al. 2023

    The Results section (‘Astrocytes and neurons are most sensitive to loss of SORL1’; page unavailable) reports proteomic profiling of SORL1-knockout iPSC-derived neurons, astrocytes, and microglia, but does not report whether retromer-component levels changed. A search for VPS35, VPS26, and retromer protein levels found discussion of retromer function, not the claimed knockout-versus-control result. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

  • SORLA deletion in iPSC-derived neurons enhances tau phosphorylation.

    “recent work indicates that SORLA deletion in iPSC-derived neurons enhances tau phosphorylation (Lee, Aylward et al. 2023).”

    From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Lee, Aylward et al. 2023

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

Flagged first, then by citations

Research works printed but not linked: 49

  1. Lambert, 2013, Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease, Nat. Genet., 45, 1452, 10.1038/ng.2802 · DOI · Paper page
  2. Bellenguez, 2022, New Insights into the Genetic Etiology of Alzheimer’s Disease and Related Dementias, Nat. Genet., 54, 412, 10.1038/s41588-022-01024-z · DOI · Paper page
  3. Pottier, 2012, High Frequency of Potentially Pathogenic SORL1 Mutations in Autosomal Dominant Early-Onset Alzheimer Disease, Mol. Psychiatr., 17, 875, 10.1038/mp.2012.15 · DOI · Paper page
  4. Vardarajan, 2015, Coding Mutations in SORL 1 and Alzheimer Disease: SORL1 Variants and AD, Ann. Neurol., 77, 215, 10.1002/ana.24305 · DOI · Paper page
  5. Holstege, 2017, Characterization of Pathogenic SORL1 Genetic Variants for Association with Alzheimer’s Disease: A Clinical Interpretation Strategy, Eur. J. Hum. Genet., 25, 973, 10.1038/ejhg.2017.87 · DOI · Paper page
  6. Scherzer, 2004, Loss of Apolipoprotein E Receptor LR11 in Alzheimer Disease, Arch. Neurol., 61, 1200, 10.1001/archneur.61.8.1200 · DOI · Paper page
  7. Dodson, 2006, LR11/SorLA Expression Is Reduced in Sporadic Alzheimer Disease but Not in Familial Alzheimer Disease, J. Neuropathol. Exp. Neurol., 65, 866, 10.1097/01.jnen.0000228205.19915.20 · DOI · Paper page
  8. Ma, 2009, Reduction of SorLA/LR11, a Sorting Protein Limiting β-Amyloid Production, in Alzheimer Disease Cerebrospinal Fluid, Arch. Neurol., 66, 448, 10.1001/archneurol.2009.22 · DOI
  9. Scheltens, 2021, Alzheimer’s Disease, Lancet, 397, 1577, 10.1016/S0140-6736(20)32205-4 · DOI · Paper page
  10. Small, 2006, Sorting through the Cell Biology of Alzheimer’s Disease: Intracellular Pathways to Pathogenesis, Neuron, 52, 15, 10.1016/j.neuron.2006.09.001 · DOI
  11. Andersen, 2005, Neuronal Sorting Protein-Related Receptor SorLA/LR11 Regulates Processing of the Amyloid Precursor Protein, Proc. Natl. Acad. Sci. USA, 102, 13461, 10.1073/pnas.0503689102 · DOI · Paper page
  12. Offe, 2006, The Lipoprotein Receptor LR11 Regulates Amyloid β Production and Amyloid Precursor Protein Traffic in Endosomal Compartments, J. Neurosci., 26, 1596, 10.1523/JNEUROSCI.4946-05.2006 · DOI · Paper page
  13. Andersen, 2016, Risk Factor SORL1: From Genetic Association to Functional Validation in Alzheimer’s Disease, Acta Neuropathol., 132, 653, 10.1007/s00401-016-1615-4 · DOI · Paper page
  14. Knupp, 2020, Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing, Cell Rep., 31, 10.1016/j.celrep.2020.107719 · DOI · Paper page
  15. Hung, 2021, SORL1 Deficiency in Human Excitatory Neurons Causes APP-Dependent Defects in the Endolysosome-Autophagy Network, Cell Rep., 35, 10.1016/j.celrep.2021.109259 · DOI · Paper page
  16. Strittmatter, 1993, Binding of Human Apolipoprotein E to Synthetic Amyloid Beta Peptide: Isoform-Specific Effects and Implications for Late-Onset Alzheimer Disease, Proc. Natl. Acad. Sci. USA, 90, 8098, 10.1073/pnas.90.17.8098 · DOI · Paper page
  17. Butt, 2022, Network Dysfunction in Cognitively Normal APOE Ε4 Carriers Is Related to Subclinical Tau, Alzheimers Dement., 18, 116, 10.1002/alz.12375 · DOI
  18. Martens, 2022, ApoE Cascade Hypothesis in the Pathogenesis of Alzheimer’s Disease and Related Dementias, Neuron, 110, 1304, 10.1016/j.neuron.2022.03.004 · DOI · Paper page
  19. Zalocusky, 2021, Neuronal ApoE Upregulates MHC-I Expression to Drive Selective Neurodegeneration in Alzheimer’s Disease, Nat. Neurosci., 24, 786, 10.1038/s41593-021-00851-3 · DOI · Paper page
  20. Taira, 2001, LR11, a Mosaic LDL Receptor Family Member, Mediates the Uptake of ApoE-Rich Lipoproteins In Vitro, ATVB, 21, 1501, 10.1161/hq0901.094500 · DOI
  21. Yajima, 2015, ApoE-Isoform-Dependent Cellular Uptake of Amyloid-β Is Mediated by Lipoprotein Receptor LR11/SorLA, Biochem. Biophys. Res. Commun., 456, 482, 10.1016/j.bbrc.2014.11.111 · DOI · Paper page
  22. Zhao, 2021, Apolipoprotein E Regulates Lipid Metabolism and α-Synuclein Pathology in Human IPSC-Derived Cerebral Organoids, Acta Neuropathol., 142, 807, 10.1007/s00401-021-02361-9 · DOI · Paper page
  23. Zhang, 2013, Rapid Single-Step Induction of Functional Neurons from Human Pluripotent Stem Cells, Neuron, 78, 785, 10.1016/j.neuron.2013.05.029 · DOI · Paper page
  24. Canals, 2018, Rapid and Efficient Induction of Functional Astrocytes from Human Pluripotent Stem Cells, Nat. Methods, 15, 693, 10.1038/s41592-018-0103-2 · DOI
  25. Muratore, 2017, Cell-Type Dependent Alzheimer’s Disease Phenotypes: Probing the Biology of Selective Neuronal Vulnerability, Stem Cell Rep., 9, 1868, 10.1016/j.stemcr.2017.10.015 · DOI
  26. Gao, 2019, Mitochondria Are Dynamically Transferring Between Human Neural Cells and Alexander Disease-Associated GFAP Mutations Impair the Astrocytic Transfer, Front. Cell. Neurosci., 13, 316, 10.3389/fncel.2019.00316 · DOI
  27. Dobrindt, 2021, Publicly Available HiPSC Lines with Extreme Polygenic Risk Scores for Modeling Schizophrenia, Complex Psychiatry, 6, 68, 10.1159/000512716 · DOI
  28. Abud, 2017, IPSC-Derived Human Microglia-like Cells to Study Neurological Diseases, Neuron, 94, 278, 10.1016/j.neuron.2017.03.042 · DOI · Paper page
  29. Lippmann, 2012, Derivation of Blood-Brain Barrier Endothelial Cells from Human Pluripotent Stem Cells, Nat. Biotechnol., 30, 783, 10.1038/nbt.2247 · DOI · Paper page
  30. Lippmann, 2014, A Retinoic Acid-Enhanced, Multicellular Human Blood-Brain Barrier Model Derived from Stem Cell Sources, Sci. Rep., 4, 4160, 10.1038/srep04160 · DOI · Paper page
  31. Park, 2019, Hypoxia-Enhanced Blood-Brain Barrier Chip Recapitulates Human Barrier Function and Shuttling of Drugs and Antibodies, Nat. Commun., 10, 2621, 10.1038/s41467-019-10588-0 · DOI
  32. Pimentel, 2017, Differential Analysis of RNA-Seq Incorporating Quantification Uncertainty, Nat. Methods, 14, 687, 10.1038/nmeth.4324 · DOI · Paper page
  33. Mishra, 2022, The Alzheimer’s Gene SORL1 Is a Regulator of Endosomal Traffic and Recycling in Human Neurons, Cell. Mol. Life Sci., 79, 162, 10.1007/s00018-022-04182-9 · DOI · Paper page
  34. Mecozzi, 2014, Pharmacological Chaperones Stabilize Retromer to Limit APP Processing, Nat. Chem. Biol., 10, 443, 10.1038/nchembio.1508 · DOI · Paper page
  35. Young, 2018, Stabilizing the Retromer Complex in a Human Stem Cell Model of Alzheimer’s Disease Reduces TAU Phosphorylation Independently of Amyloid Precursor Protein, Stem Cell Rep., 10, 1046, 10.1016/j.stemcr.2018.01.031 · DOI · Paper page
  36. Mathys, 2019, Single-Cell Transcriptomic Analysis of Alzheimer’s Disease, Nature, 570, 332, 10.1038/s41586-019-1195-2 · DOI · Paper page
  37. Mishra, S.; Knupp, A.; Kinoshita, C.; Martinez, R.; Theofilas, P.; Young, J.. Pharmacologic Stabilization of Retromer Rescues Endosomal Pathology Induced by Defects in the Alzheimer’s Gene SORL1. https://doi.org/10.1101/2022.07.31.502217. · DOI
  38. Liu, 2020, Multi-Omic Comparison of Alzheimer’s Variants in Human ESC–Derived Microglia Reveals Convergence at APOE, J. Exp. Med., 217, 10.1084/jem.20200474 · DOI · Paper page
  39. Sager, 2007, Neuronal LR11/SorLA Expression Is Reduced in Mild Cognitive Impairment, Ann. Neurol., 62, 640, 10.1002/ana.21190 · DOI · Paper page
  40. Singh, 2006, Transforming Growth Factor-β–Induced Expression of the Apolipoprotein E Gene Requires c-Jun N-Terminal Kinase, P38 Kinase, and Casein Kinase 2, ATVB, 26, 1323, 10.1161/01.ATV.0000220383.19192.55 · DOI
  41. Luo, 2017, Signaling Cross Talk between TGF-β/Smad and Other Signaling Pathways, Cold Spring Harb. Perspect. Biol., 9, a022137, 10.1101/cshperspect.a022137 · DOI
  42. McQuin, 2018, CellProfiler 3.0: Next-Generation Image Processing for Biology, PLoS Biol., 16, 10.1371/journal.pbio.2005970 · DOI
  43. Young, 2015, Elucidating Molecular Phenotypes Caused by the SORL1 Alzheimer’s Disease Genetic Risk Factor Using Human Induced Pluripotent Stem Cells, Cell Stem Cell, 16, 373, 10.1016/j.stem.2015.02.004 · DOI
  44. Muratore, 2014, Comparison and Optimization of HiPSC Forebrain Cortical Differentiation Protocols, PLoS One, 9, 10.1371/journal.pone.0105807 · DOI
  45. Chou, 2023, INPP5D/SHIP1 Regulates Inflammasome Activation in Human Microglia; preprint, Neuroscience
  46. Bray, 2016, Near-Optimal Probabilistic RNA-Seq Quantification, Nat. Biotechnol., 34, 525, 10.1038/nbt.3519 · DOI · Paper page
  47. Wu, 2021, ClusterProfiler 4.0: A Universal Enrichment Tool for Interpreting Omics Data, Innovation, 2
  48. Wickham, 2016, 10.1007/978-3-319-24277-4 · DOI
  49. Pérez-Silva, 2018, NVenn: Generalized, Quasi-Proportional Venn and Euler Diagrams, Bioinformatics, 34, 2322, 10.1093/bioinformatics/bty109 · DOI

Cited by

Sorted by citations

Metadata

Authors
Lee, H., Aylward, A. J., Pearse, R. V., Lish, A. M., Hsieh, Y.-C., Augur, Z. M., Benoit, C. R., Chou, V., Knupp, A., Pan, C., Goberdhan, S., Duong, D. M., Seyfried, N. T., Bennett, D. A., Taga, M. F., Huynh, K., Arnold, M., Meikle, P. J., De Jager, P. L., Menon, V., Young, J. E., & Young-Pearse, T. L.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2023-08
Volume
42
Issue
8
Pages
112994
ISSN
2211-1247
DOI
10.1016/j.celrep.2023.112994
PMC
PMC10568487
Cited by
58
References
14
Language
en
Licence
Funders
  • National Institutes of Health
  • National Institute on Aging (F31AG063399, R01AG055909, U01AG061356, U01AG061359, U01AG072572)
  • National Institute of Neurological Disorders and Stroke (RF1NS117446)

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