The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Alzheimer's vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling
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 endosomal network is a key biological pathway affected in neurodegenerative pathology.
“These studies, alongside clinical evidence [8][9][10][11][12][13][14], highlight the endosomal network as a key biological pathway affected in neurodegenerative pathology.”
From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [12]
The Introduction identifies endosomal trafficking as a pathogenic pathway in Alzheimer’s disease, and the Discussion links impaired endosomal recycling to its pathology. The claim extends that finding to neurodegenerative pathology generally; the paper’s substantive discussion here is specific to Alzheimer’s disease. (LLM, conf=0.83)
Experimental — accuracy not yet measuredDeletion of a neuron-specific VPS26 isoform (VPS26b) in mouse brain is associated with decreased total and cell-surface SORLA levels, as well as increased murine brain Aβ and CSF tau.
“Interestingly, deletion of a neuron-specific VPS26 isoform (VPS26b) in mouse brain is associated with decreased total and cell-surface SORLA levels, as well as increased murine brain Aβ and CSF tau (Simoes, Guo et al. 2021), implicating interdependent roles for retromer, SORLA and AD pathology.”
From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Simoes, Guo et al. 2021
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
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
The Alzheimer’s disease neuroimaging initiative (ADNI): MRI methods
Jack, C. R., Bernstein, M. A., Fox, N. C., Thompson, P., Alexander, G., Harvey, D., Borowski, B., Britson, P. J., L. Whitwell, J., Ward, C., et al. (2008) · Journal of Magnetic Resonance Imaging · doi:10.1002/jmri.21049 · Cited by 4,347
Profound Loss of Layer II Entorhinal Cortex Neurons Occurs in Very Mild Alzheimer’s Disease
Gómez-Isla, T., Price, J. L., McKeel Jr., D. W., Morris, J. C., Growdon, J. H., & Hyman, B. T. (1996) · The Journal of Neuroscience · doi:10.1523/jneurosci.16-14-04491.1996 · Cited by 1,796 · cited 1×
“A range of studies have established that the border zone between the entorhinal and perirhinal cortices, termed the trans-entorhinal cortex (TEC) in clinical literature, is selectively vulnerable to AD (Braak and Braak, 1991; Gomez-Isla et al., 1996; Khan et al., 2014; Adams et al., 2019).”
Recycling Endosomes Supply AMPA Receptors for LTP
Park, M., Penick, E. C., Edwards, J. G., Kauer, J. A., & Ehlers, M. D. (2004) · Science · doi:10.1126/science.1102026 · Cited by 730
Khan, U. A., Liu, L., Provenzano, F. A., Berman, D. E., Profaci, C. P., Sloan, R., Mayeux, R., Duff, K. E., & Small, S. A. (2014) · Nature Neuroscience · doi:10.1038/nn.3606 · Cited by 561
Self-citationRetromer: A Master Conductor of Endosome Sorting
Burd, C., & Cullen, P. J. (2014) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016774 · Cited by 435
Alamed, J., Wilcock, D. M., Diamond, D. M., Gordon, M. N., & Morgan, D. (2006) · Nature Protocols · doi:10.1038/nprot.2006.275 · Cited by 256
Muhammad, A., Flores, I., Zhang, H., Yu, R., Staniszewski, A., Planel, E., Herman, M., Ho, L., Kreber, R., Honig, L. S., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0802545105 · Cited by 248
Self-citationCortical tau deposition follows patterns of entorhinal functional connectivity in aging
Adams, J. N., Maass, A., Harrison, T. M., Baker, S. L., & Jagust, W. J. (2019) · eLife · doi:10.7554/elife.49132 · Cited by 160
Flagged first, then by citations
Research works printed but not linked: 66
- Andersen, 2021, In vivo evidence that SORL1, encoding the endosomal recycling receptor SORLA, can function as a casual gene in Alzheimer’s Disease, bioRxiv
- Attar, 2010, The retromer complex, Adv. Enzyme Regul., 50, 216, 10.1016/j.advenzreg.2009.10.002 · DOI
- Avants, 2011, A reproducible evaluation of ANTs similarity metric performance in brain image registration, Neuroimage, 54, 2033, 10.1016/j.neuroimage.2010.09.025 · DOI · Paper page
- Barker, 2011, When is the hippocampus involved in recognition memory?, J. Neurosci., 31, 10721, 10.1523/JNEUROSCI.6413-10.2011 · DOI
- Bateman, 2007, Fluctuations of CSF amyloid-beta levels: Implications for a diagnostic and therapeutic biomarker, Neurology, 68, 666, 10.1212/01.wnl.0000256043.50901.e3 · DOI · Paper page
- Bhalla, 2012, The location and trafficking routes of the neuronal retromer and its role in amyloid precursor protein transport, Neurobiol. Dis., 47, 126, 10.1016/j.nbd.2012.03.030 · DOI · Paper page
- 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
- Bota, 2015, Architecture of the cerebral cortical association connectome underlying cognition, Proc. Natl. Acad. Sci. U S A, 112, E2093, 10.1073/pnas.1504394112 · DOI · Paper page
- Bugarcic, 2011, Vps26A and Vps26B subunits define distinct retromer complexes, Traffic, 12, 1759, 10.1111/j.1600-0854.2011.01284.x · DOI
- Cepeda-Prado, 2012, R6/2 Huntington's disease mice develop early and progressive abnormal brain metabolism and seizures, J. Neurosci., 32, 6456, 10.1523/JNEUROSCI.0388-12.2012 · DOI
- Chou, 2011, Robust automatic rodent brain extraction using 3-D pulse-coupled neural networks (PCNN), IEEE Trans. Image Process., 20, 2554, 10.1109/TIP.2011.2126587 · DOI
- Choy, 2014, Retromer mediates a discrete route of local membrane delivery to dendrites, Neuron, 82, 55, 10.1016/j.neuron.2014.02.018 · DOI · Paper page
- Criscuolo, 2015, BDNF prevents amyloid-dependent impairment of LTP in the entorhinal cortex by attenuating p38 MAPK phosphorylation, Neurobiol. Aging, 36, 1303, 10.1016/j.neurobiolaging.2014.11.016 · DOI
- Ehlers, 2000, Reinsertion or degradation of AMPA receptors determined by activity-dependent endocytic sorting, Neuron, 28, 511, 10.1016/S0896-6273(00)00129-X · DOI · Paper page
- Fischl, 2000, Measuring the thickness of the human cerebral cortex from magnetic resonance images, Proc. Natl. Acad. Sci. U S A, 97, 11050, 10.1073/pnas.200033797 · DOI
- Fischl, 1999, Cortical surface-based analysis. II: Inflation, flattening, and a surface-based coordinate system, Neuroimage, 9, 195, 10.1006/nimg.1998.0396 · DOI · Paper page
- 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
- 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
- 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
- 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
- Kennedy, 2011, Mechanisms and function of dendritic exocytosis, Neuron, 69, 856, 10.1016/j.neuron.2011.02.032 · DOI · Paper page
- Kerr, 2005, A novel mammalian retromer component, Vps26B, Traffic, 6, 991, 10.1111/j.1600-0854.2005.00328.x · DOI · Paper page
- Kim, 2008, Identification of novel retromer complexes in the mouse testis, Biochem. Biophys. Res. Commun., 375, 16, 10.1016/j.bbrc.2008.07.067 · DOI
- Kim, 2010, Implication of mouse Vps26b-Vps29-Vps35 retromer complex in sortilin trafficking, Biochem. Biophys. Res. Commun., 403, 167, 10.1016/j.bbrc.2010.10.121 · DOI
- Knupp, 2020, Depletion of the AD risk gene SORL1 selectively Impairs neuronal endosomal traffic independent of amyloidogenic APP processing, Cell Rep., 31, 107719, 10.1016/j.celrep.2020.107719 · DOI · Paper page
- Kovtun, 2018, Structure of the membrane-assembled retromer coat determined by cryo-electron tomography, Nature, 561, 561, 10.1038/s41586-018-0526-z · DOI · Paper page
- Kwart, 2019, A large panel of isogenic APP and PSEN1 mutant human iPSC Neurons reveals shared endosomal abnormalities mediated by APP beta-CTFs, not abeta, Neuron, 104, 256, 10.1016/j.neuron.2019.07.010 · DOI
- Ma, 2008, Differential induction of long-term potentiation in the horizontal versus columnar superficial connections to layer II cells of the entorhinal cortex, Neural Plast., 2008, 814815, 10.1155/2008/814815 · DOI
- Maia, 2013, Changes in amyloid-beta and Tau in the cerebrospinal fluid of transgenic mice overexpressing amyloid precursor protein, Sci. Transl. Med., 5, 194re2, 10.1126/scitranslmed.3006446 · DOI · Paper page
- Mecozzi, 2014, Pharmacological chaperones stabilize retromer to limit APP processing, Nat. Chem. Biol., 10, 443, 10.1038/nchembio.1508 · DOI · Paper page
- Mirra, 1991, The consortium to establish a registry for Alzheimer's disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer's disease, Neurology, 41, 479, 10.1212/WNL.41.4.479 · DOI · Paper page
- Morabito, 2014, Hyperleucinemia causes hippocampal retromer deficiency linking diabetes to Alzheimer's disease, Neurobiol. Dis., 65, 188, 10.1016/j.nbd.2013.12.017 · DOI
- Moreno, 2006, Longitudinal mapping of mouse cerebral blood volume with MRI, NMR Biomed., 19, 535, 10.1002/nbm.1022 · DOI
- 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
- 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
- Pensalfini, 2020, Endosomal dysfunction induced by directly overactivating Rab5 recapitulates prodromal and neurodegenerative features of Alzheimer's disease, Cell Rep., 33, 108420, 10.1016/j.celrep.2020.108420 · DOI
- Qureshi, 2019, Retromer repletion with AAV9-VPS35 restores endosomal function in the mouse hippocampus, bioRxiv, 618496
- Qureshi, 2020, Retromer combinatorials for gene-therapy across a spectrum of neurological diseases, bioRxiv
- Rogaeva, 2007, The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease, Nat. Genet., 39, 168, 10.1038/ng1943 · DOI · Paper page
- Rojas, 2008, Regulation of retromer recruitment to endosomes by sequential action of Rab5 and Rab7, J. Cell Biol., 183, 513, 10.1083/jcb.200804048 · DOI · Paper page
- Rojas, 2008, Regulation of retromer recruitment to endosomes by sequential action of Rab5 and Rab7, J Cell Biol., 183, 513, 10.1083/jcb.200804048 · DOI · Paper page
- Sabuncu, 2009, Asymmetric Image-Template Registration, Med. Image Comput. Comput. Assist. Interv., 12, 565
- Scheltens, 2021, Alzheimer's disease, Lancet, 397, 1577, 10.1016/S0140-6736(20)32205-4 · DOI · Paper page
- Schobel, 2013, Imaging patients with psychosis and a mouse model establishes a spreading pattern of hippocampal dysfunction and implicates glutamate as a driver, Neuron, 78, 81, 10.1016/j.neuron.2013.02.011 · DOI · Paper page
- Seaman, 2005, Recycle your receptors with retromer, Trends Cell Biol., 15, 68, 10.1016/j.tcb.2004.12.004 · DOI · Paper page
- Seaman, 2012, The retromer complex - endosomal protein recycling and beyond, J. Cell Sci., 125, 4693
- Selkoe, 2002, Alzheimer's disease is a synaptic failure, Science, 298, 789, 10.1126/science.1074069 · DOI · Paper page
- Simoes, 2020, Tau and other proteins found in Alzheimer's disease spinal fluid are linked to retromer-mediated endosomal traffic in mice and humans, Sci. Transl. Med., 12, eaba6334, 10.1126/scitranslmed.aba6334 · DOI · Paper page
- Singh, 2006, Spatial patterns of cortical thinning in mild cognitive impairment and Alzheimer's disease, Brain, 129, 2885, 10.1093/brain/awl256 · DOI · Paper page
- 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
- Small, 2005, Model-guided microarray implicates the retromer complex in Alzheimer's disease, Ann. Neurol., 58, 909, 10.1002/ana.20667 · DOI · Paper page
- Small, 2015, Retromer in Alzheimer disease, Parkinson disease and other neurological disorders, Nat. Rev. Neurosci., 16, 126, 10.1038/nrn3896 · DOI · Paper page
- Small, 2011, A pathophysiological framework of hippocampal dysfunction in ageing and disease, Nat. Rev. Neurosci., 12, 585, 10.1038/nrn3085 · DOI
- Small, 2017, Endosomal traffic jams represent a pathogenic hub and therapeutic target in Alzheimer's disease, Trends Neurosci., 40, 592, 10.1016/j.tins.2017.08.003 · DOI · Paper page
- Small, 2019, A network explanation of Alzheimer's regional vulnerability, Cold Spring Harb. Symp. Quant Biol., 83, 193, 10.1101/sqb.2018.83.036889 · DOI
- Temkin, 2017, The retromer supports AMPA receptor trafficking during LTP, Neuron, 94, 74, 10.1016/j.neuron.2017.03.020 · DOI · Paper page
- Thonberg, 2017, Identification and description of three families with familial Alzheimer disease that segregate variants in the SORL1 gene, Acta Neuropathol. Commun., 5, 43, 10.1186/s40478-017-0441-9 · DOI · Paper page
- Tian, 2015, VPS35-deficiency results in an impaired AMPA receptor trafficking and decreased dendritic spine maturation, Mol. Brain, 8, 70, 10.1186/s13041-015-0156-4 · DOI · Paper page
- Truschel, 2009, ESCRT-I function is required for Tyrp1 transport from early endosomes to the melanosome limiting membrane, Traffic, 10, 1318, 10.1111/j.1600-0854.2009.00955.x · DOI
- Vardarajan, 2012, Identification of Alzheimer disease-associated variants in genes that regulate retromer function, Neurobiol. Aging, 33, 10.1016/j.neurobiolaging.2012.04.020 · DOI · Paper page
- Vonsattel, 1995, An improved approach to prepare human brains for research, J. Neuropathol. Exp. Neurol., 54, 42, 10.1097/00005072-199501000-00006 · DOI
- Wang, 2008, Myosin Vb mobilizes recycling endosomes and AMPA receptors for postsynaptic plasticity, Cell, 135, 535, 10.1016/j.cell.2008.09.057 · DOI · Paper page
- Wilson, 2013, Lateral entorhinal cortex is critical for novel object-context recognition, Hippocampus, 23, 352, 10.1002/hipo.22095 · DOI
- 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
- Zamanillo, 1999, Importance of AMPA receptors for hippocampal synaptic plasticity but not for spatial learning, Science, 284, 1805, 10.1126/science.284.5421.1805 · DOI · Paper page
- Zetterberg, 2017, Review: Tau in biofluids - relation to pathology, imaging and clinical features, Neuropathol. Appl. Neurobiol., 43, 194, 10.1111/nan.12378 · DOI · Paper page
Cited by
Sorted by citations
Receptor Recycling by Retromer
Carosi, J. M., Denton, D., Kumar, S., & Sargeant, T. J. (2023) · Molecular and Cellular Biology · doi:10.1080/10985549.2023.2222053 · Cited by 36
PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity
Rivero-Ríos, P., Uygun, T., Chavis, G. D., Lee, H., Duan, B., Sutton, M. A., & Weisman, L. S. (2025) · Journal of Cell Biology · doi:10.1083/jcb.202411198 · Cited by 1
SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain
Huang, H., Shi, C. H., Yang, W., Piña-Crespo, J. C., Bhatnagar, J., Curatolo, J., Murad, R., Shah, P., Campos, A., Houser, A., et al. (2026) · Science Advances · doi:10.1126/sciadv.aed6825 · Cited by 1
Jones, E., Adams, H., Chen, K.-E., Maroof, F., Ibbotson, T. M., Nakamura, Y., Banks, P. J., Healy, M. D., Lewis, P. A., Heesom, K. J., et al. (2026) · doi:10.64898/2026.05.14.724903
Metadata
- Authors
- Simoes, S., Guo, J., Buitrago, L., Qureshi, Y. H., Feng, X., Kothiya, M., Cortes, E., Patel, V., Kannan, S., Kim, Y.-H., Chang, K.-T., Hussaini, S. A., Moreno, H., Di Paolo, G., Andersen, O. M., & Small, S. A.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2021-12
- Volume
- 37
- Issue
- 13
- Pages
- 110182
- ISSN
- 2211-1247
- PMC
- PMC8792909
- Cited by
- 68
- References
- 9
- Language
- en
- Licence
- Funders
- Eli Lilly and Company
- Denali Therapeutics
- Genentech
- H. Lundbeck A/S
- Merck
- Janssen Research and Development
- Northern California Institute for Research and Education
- National Institute of Biomedical Imaging and Bioengineering
- Fujirebio US
- GE Healthcare
- National Institutes of Health (AG034618, AG035015, AG051556, NS056049, P30AG066462, U01 AG024904)
- F. Hoffmann-La Roche
- DOD (W81XWH-12-2-0012)
- Alzheimer's Disease Neuroimaging Initiative
- National Institute on Aging
- University of Southern California
- Alzheimer's Disease Research Center, Emory University
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