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Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing

Knupp, Allison, Mishra, Swati, Martinez, Refugio, Braggin, Jacquelyn E., Szabo, Marcell, Kinoshita, Chizuru, Hailey, Dale W., Small, Scott A., Jayadev, Suman, Young, Jessica E.·2020·Cell Reports
DOI 10.1016/j.celrep.2020.107719PMC PMC7409533

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  • Loss of SORLA causes endo-lysosomal defects in neurons, including in endosomal recycling, autophagy, and lysosome function, resulting in increased secretion of toxic Aβ species and impaired synaptic activity.

    “Studies investigating the role of SORLA in ad pathogenesis have extensively focused on neurons and revealed that loss of SORLA causes endo‐lysosomal defects in neurons, specifically in endosomal recycling, autophagy, and lysosome function, ultimately resulting in increased secretion of toxic Aβ species and impaired synaptic activity in neurons (Andersen et al. 2022; Hung et al. 2021; Knupp et al.”

    From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Knupp et al. 2020

    The Introduction and the section on APP trafficking report enlarged endosomes and altered APP transport in SORL1-deficient neurons. The APP-processing section reports increased secretion of Aβ1–40 and Aβ1–42. The paper does not establish the claimed defects in autophagy, lysosome function, or synaptic activity, nor does it test whether the secreted Aβ is toxic; its trafficking findings also do not specifically establish impaired endosomal recycling. Page numbers were not available in our copy. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • 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 Knupp et al. 2020

    The Results sections on endosome size and APP trafficking (page numbers unavailable) report enlarged early endosomes and altered endo-lysosomal trafficking in SORL1-deficient neurons. The passages do not establish the attributed changes in gene expression or impaired neuronal function; searches for those outcomes found no supporting results in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • SORLA deletion as well as AD-associated Y1816C, G511R, E270K and Y141C variants can promote endosomal enlargement and dysregulated trafficking of targets such as APP and GLUA1 in iPSC-derived neurons.

    “SORLA deletion as well as AD-associated Y1816C, G511R, E270K and Y141C variants can promote endosomal enlargement (Knupp, Mishra et al. 2020, Hung, Tuck et al. 2021, Mishra, Knupp et al. 2023, Jensen, Raska et al. 2024) and dysregulated trafficking of targets such as APP and GLUA1 in iPSC-derived neurons (Mishra, Knupp et al. 2022).”

    From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Knupp, Mishra et al. 2020

  • We did not observe differences in the size of early endosomes between SORL1 WT and SORL1 KO hMGLs.

    “We did not observe differences in the size of early endosomes between SORL1 WT and SORL1 KO hMGLs (Knupp et al. 2020) but have documented lysosomal enlargement in SORL1 KO microglia (Mishra 2024).”

    From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Knupp et al. 2020

  • SORLA deletion results in endosomal and lysosomal defects in iPSC-derived neurons.

    “Previous groups have reported that SORLA deletion results in endosomal (Knupp, Mishra et al. 2020, Hung, Tuck et al. 2021), as well as lysosomal defects (Hung, Tuck et al. 2021) in iPSC-derived neurons.”

    From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Knupp, Mishra et al. 2020

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Research works printed but not linked: 40

  1. Andersen, 2005, Neuronal sorting protein-related receptor sorLA/LR11 regulates processing of the amyloid precursor protein, Proc. Natl. Acad. Sci. U S A, 102, 13461, 10.1073/pnas.0503689102 · DOI · Paper page
  2. Bettens, 2008, SORL1 is genetically associated with increased risk for late-onset Alzheimer disease in the Belgian population, Hum. Mutat., 29, 769, 10.1002/humu.20725 · DOI
  3. Bolte, 2006, A guided tour into subcellular colocalization analysis in light microscopy, J. Microsc., 224, 213, 10.1111/j.1365-2818.2006.01706.x · DOI
  4. Caglayan, 2014, Lysosomal sorting of amyloid-β by the SORLA receptor is impaired by a familial Alzheimer’s disease mutation, Sci. Transl. Med., 6, 223ra20, 10.1126/scitranslmed.3007747 · DOI · Paper page
  5. 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
  6. 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
  7. Dumanis, 2015, Distinct functions for anterograde and retrograde sorting of SORLA in amyloidogenic processes in the brain, J. Neurosci., 35, 12703, 10.1523/JNEUROSCI.0427-15.2015 · DOI
  8. Fjorback, 2012, Retromer binds the FANSHY sorting motif in SorLA to regulate amyloid precursor protein sorting and processing, J. Neurosci., 32, 1467, 10.1523/JNEUROSCI.2272-11.2012 · DOI · Paper page
  9. Glerup, 2013, SorLA controls neurotrophic activity by sorting of GDNF and its receptors GFRα1 and RET, Cell Rep., 3, 186, 10.1016/j.celrep.2012.12.011 · DOI · Paper page
  10. Hermans-Borgmeyer, 1998, Unique expression pattern of a novel mosaic receptor in the developing cerebral cortex, Mech. Dev., 70, 65, 10.1016/S0925-4773(97)00177-9 · DOI
  11. Herskowitz, 2012, GGA1-mediated endocytic traffic of LR11/SorLA alters APP intracellular distribution and amyloid-β production, Mol. Biol. Cell, 23, 2645, 10.1091/mbc.e12-01-0014 · DOI
  12. 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
  13. 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
  14. Kaur, 2018, Early endosome morphology in health and disease, Adv. Exp. Med. Biol., 1074, 335, 10.1007/978-3-319-75402-4_41 · DOI
  15. Kim, 2016, Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer’s disease, Mol. Psychiatry, 21, 707, 10.1038/mp.2015.97 · DOI · Paper page
  16. Klinger, 2011, SorLA regulates the activity of lipoprotein lipase by intracellular trafficking, J. Cell Sci., 124, 1095, 10.1242/jcs.072538 · DOI
  17. Kwart, 2019, A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP β-CTFs, not Aβ, Neuron, 104, 1022, 10.1016/j.neuron.2019.11.010 · DOI · Paper page
  18. Ma, 2009, Reduction of SorLA/LR11, a sorting protein limiting beta-amyloid production, in Alzheimer disease cerebrospinal fluid, Arch. Neurol., 66, 448, 10.1001/archneurol.2009.22 · DOI
  19. Martini, 2019, Amyloid-beta impairs TOM1-mediated IL-1R1 signaling, Proc. Natl. Acad. Sci. U S A, 116, 21198, 10.1073/pnas.1914088116 · DOI
  20. McQuin, 2018, CellProfiler 3.0: Next-generation image processing for biology, PLoS Biol., 16, e2005970, 10.1371/journal.pbio.2005970 · DOI
  21. Mecozzi, 2014, Pharmacological chaperones stabilize retromer to limit APP processing, Nat. Chem. Biol., 10, 443, 10.1038/nchembio.1508 · DOI · Paper page
  22. Mehmedbasic, 2015, SorLA complement-type repeat domains protect the amyloid precursor protein against processing, J. Biol. Chem., 290, 3359, 10.1074/jbc.M114.619940 · DOI
  23. Netzer, 2017, Gleevec shifts APP processing from a β-cleavage to a nonamyloidogenic cleavage, Proc. Natl. Acad. Sci. U S A, 114, 1389, 10.1073/pnas.1620963114 · DOI
  24. Nielsen, 2007, Sorting by the cytoplasmic domain of the amyloid precursor protein binding receptor SorLA, Mol. Cell. Biol., 27, 6842, 10.1128/MCB.00815-07 · DOI · Paper page
  25. Offe, 2006, The lipoprotein receptor LR11 regulates amyloid beta production and amyloid precursor protein traffic in endosomal compartments, J. Neurosci., 26, 1596, 10.1523/JNEUROSCI.4946-05.2006 · DOI · Paper page
  26. Pottier, 2012, High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease, Mol. Psychiatry, 17, 875, 10.1038/mp.2012.15 · DOI · Paper page
  27. Reitz, 2011, Meta-analysis of the association between variants in SORL1 and Alzheimer disease, Arch. Neurol., 68, 99, 10.1001/archneurol.2010.346 · DOI · Paper page
  28. Rogaeva, 2007, The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease, Nat. Genet., 39, 168, 10.1038/ng1943 · DOI · Paper page
  29. Rose, 2018, Leptomeninges-derived induced pluripotent stem cells and directly converted neurons from autopsy cases with varying neuropathologic backgrounds, J. Neuropathol. Exp. Neurol., 77, 353, 10.1093/jnen/nly013 · DOI
  30. Sager, 2007, Neuronal LR11/sorLA expression is reduced in mild cognitive impairment, Ann. Neurol., 62, 640, 10.1002/ana.21190 · DOI · Paper page
  31. Schindelin, 2012, Fiji: an open-source platform for biological-image analysis, Nat. Methods, 9, 676, 10.1038/nmeth.2019 · DOI · Paper page
  32. Skovronsky, 2000, Protein kinase C-dependent alpha-secretase competes with beta-secretase for cleavage of amyloid-beta precursor protein in the trans-golgi network, J. Biol. Chem., 275, 2568, 10.1074/jbc.275.4.2568 · DOI
  33. 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
  34. Tamayev, 2012, β- but not γ-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
  35. Vagnozzi, 2019, Endosomal sorting and trafficking, the retromer complex and neurodegeneration, Mol. Psychiatry, 24, 857, 10.1038/s41380-018-0221-3 · DOI · Paper page
  36. Ventura, 2004, Cre-lox-regulated conditional RNA interference from transgenes, Proc. Natl. Acad. Sci. U S A, 101, 10380, 10.1073/pnas.0403954101 · DOI
  37. Xu, 2016, Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegeneration, J. Clin. Invest., 126, 1815, 10.1172/JCI82409 · DOI
  38. 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
  39. 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 Reports, 10, 1046, 10.1016/j.stemcr.2018.01.031 · DOI · Paper page
  40. Yuan, 2011, Cell-surface marker signatures for the isolation of neural stem cells, glia and neurons derived from human pluripotent stem cells, PLoS ONE, 6, e17540, 10.1371/journal.pone.0017540 · DOI

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Metadata

Authors
Knupp, A., Mishra, S., Martinez, R., Braggin, J. E., Szabo, M., Kinoshita, C., Hailey, D. W., Small, S. A., Jayadev, S., & Young, J. E.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2020-06
Volume
31
Issue
9
Pages
107719
ISSN
2211-1247
DOI
10.1016/j.celrep.2020.107719
PMC
PMC7409533
Cited by
165
References
14
Language
en
Licence
Funders
  • BrightFocus Foundation (A2018656S, T32AG052354)
  • National Institutes of Health (R01AG062148, T32AG052354)

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