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The microglial lysosomal system in Alzheimer’s disease: Guardian against proteinopathy

Van Acker, Zoë P., Perdok, Anika, Bretou, Marine, Annaert, Wim·2021·Ageing Research Reviews
DOI 10.1016/j.arr.2021.101444
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  • There are several mechanisms by which SORLA-related trafficking can affect pro-inflammatory responses that are important in AD.

    “As aberrant lysosome function can negatively impact the neuroimmune response of microglia (Quick et al. 2023; Van Acker et al. 2021), our data, along with that of Ovesen et al., suggests that there are several mechanisms by which SORLA‐related trafficking can affect pro‐inflammatory responses that are important in ad.”

    From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Van Acker et al. 2021

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Research works printed but not linked: 121

  1. Aikawa, 2019, ABCA7 haplodeficiency disturbs microglial immune responses in the mouse brain, PNAS U. S. A., 116, 23790, 10.1073/pnas.1908529116 · DOI
  2. Allendorf, 2020, Activated microglia desialylate their surface, stimulating complement receptor 3‐mediated phagocytosis of neurons, Glia, 68, 989, 10.1002/glia.23757 · DOI
  3. Angelova, 2018, Altered processing of β-Amyloid in SH-SY5Y cells induced by model senescent microglia, ACS Chem. Neurosci., 9, 3137, 10.1021/acschemneuro.8b00334 · DOI
  4. Antonyan, 2018, Concerted action of dipeptidyl peptidase IV and glutaminyl cyclase results in formation of pyroglutamate-modified amyloid peptides in vitro, Neurochem. Int., 113, 112, 10.1016/j.neuint.2017.12.001 · DOI
  5. Asai, 2015, Depletion of microglia and inhibition of exosome synthesis halt tau propagation, Nat. Neurosci., 18, 1584, 10.1038/nn.4132 · DOI · Paper page
  6. Askew, 2017, Coupled proliferation and apoptosis maintain the rapid turnover of microglia in the adult brain, Cell Rep., 18, 391, 10.1016/j.celrep.2016.12.041 · DOI · Paper page
  7. Biessels, 2020, Understanding multifactorial brain changes in type 2 diabetes: a biomarker perspective, Lancet Neurol., 19, 699, 10.1016/S1474-4422(20)30139-3 · DOI
  8. Blanco-Luquin, 2018, PLD3 epigenetic changes in the hippocampus of Alzheimer’s disease, Clin. Epigenetics, 10, 116, 10.1186/s13148-018-0547-3 · DOI
  9. Bode, 2017, Ion channel formation by Amyloid-β42 oligomers but not Amyloid-β40 in cellular membranes, JBC, 292, 1404, 10.1074/jbc.M116.762526 · DOI
  10. Bohne, 2004, Cleavage of AL amyloid proteins and AL amyloid deposits by cathepsins B, K, and L. J, Pathol., 203, 528, 10.1002/path.1553 · DOI
  11. Bordeleau, 2019, Microglia along sex lines: from brain colonization, maturation and function, to implication in neurodevelopmental disorders, Semin. Cell Dev. Biol., 94, 152, 10.1016/j.semcdb.2019.06.001 · DOI · Paper page
  12. Bretou, 2017, Lysosome signaling controls the migration of dendritic cells, Sci. Immunol., 2
  13. Bsibsi, 2002, Broad expression of toll-like receptors in the human central nervous system, J. Neuropathol. Exp. Neurol., 61, 1013, 10.1093/jnen/61.11.1013 · DOI
  14. Burns, 2020, Differential accumulation of storage bodies with aging defines discrete subsets of microglia in the healthy brain, Elife, 9, 10.7554/eLife.57495 · DOI
  15. Cacace, 2020, A family-based genetic study identifies mutations in TLR9 impairing receptor activation: a role for innate immunity in AD pathogenesis, Alzheimer’s Dement., 10.1002/alz.047212 · DOI
  16. Cappel, 2021, Quantification and characterization of the 5′ exonuclease activity of the lysosomal nuclease PLD3 by a novel cell-based assay, JBC, 296, 10.1074/jbc.RA120.015867 · DOI
  17. Chakraborty, 2017, High lumenal chloride in the lysosome is critical for lysosome function, Elife, 6
  18. Chali, 2019, Lipid markers and related transcripts during excitotoxic neurodegeneration in kainate‐treated mice, Eur. J. Neurosci., 50
  19. Crotti, 2019, BIN1 favors the spreading of Tau via extracellular vesicles, Sci. Rep., 9, 10.1038/s41598-019-45676-0 · DOI · Paper page
  20. Del-Aguila, 2019, A single-nuclei RNA sequencing study of Mendelian and sporadic AD in the human brain, Alzheimers Res. Ther., 11, 71, 10.1186/s13195-019-0524-x · DOI · Paper page
  21. Delgado, 2008, Toll-like receptors control autophagy, EMBO J., 27, 1110, 10.1038/emboj.2008.31 · DOI · Paper page
  22. Duus, 2010, Direct interaction between CD91 and C1q, FEBS J., 277, 3526, 10.1111/j.1742-4658.2010.07762.x · DOI
  23. Escamilla-Ayala, 2020, Contribution of the Presenilins in the cell biology, structure and function of γ-secretase, Semin. Cell Dev. Biol., 10.1016/j.semcdb.2020.02.005 · DOI
  24. Fitzgerald, 2018, A system of cytokines encapsulated in ExtraCellular vesicles, Sci. Rep., 8, 10.1038/s41598-018-27190-x · DOI
  25. Flowers, 2017, Proteomic analysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response, J. Neuroinflammation, 14, 96, 10.1186/s12974-017-0840-7 · DOI
  26. Frank, 2019, Microglia: neuroimmune-sensors of stress, Semin. Cell Dev. Biol., 94, 176, 10.1016/j.semcdb.2019.01.001 · DOI
  27. Franklin, 2014, The adaptor ASC has extracellular and “prionoid” activities that propagate inflammation, Nat. Immunol., 15, 727, 10.1038/ni.2913 · DOI · Paper page
  28. Füger, 2017, Microglia turnover with aging and in an Alzheimer’s model via long-term in vivo single-cell imaging, Nat. Neurosci., 20, 1371, 10.1038/nn.4631 · DOI · Paper page
  29. Fujikura, 2019, CD14 and toll-like receptor 4 promote fibrillar a beta(42) uptake by microglia through a clathrin-mediated pathway, J. Alzheimers Dis., 68, 323, 10.3233/JAD-180904 · DOI
  30. Gan, 2019, The lysosomal GPCR-like protein GPR137B regulates Rag and mTORC1 localization and activity, Nat. Cell Biol., 21, 614, 10.1038/s41556-019-0321-6 · DOI
  31. Gao, 2020, Cholesterol modulates the formation of the aβ ion channel in lipid bilayers, Biochemistry, 59, 992, 10.1021/acs.biochem.9b00968 · DOI
  32. García-Revilla, 2019, Reformulating pro-oxidant microglia in neurodegeneration, J. Clin. Med., 8, E1719, 10.3390/jcm8101719 · DOI
  33. Gavin, 2018, PLD3 and PLD4 are single-stranded acid exonucleases that regulate endosomal nucleic-acid sensing, Nat. Immunol., 19, 942, 10.1038/s41590-018-0179-y · DOI
  34. Götzl, 2019, Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism, EMBO Mol. Med., 11
  35. Guerreiro, 2013, TREM2 variants in Alzheimer’s disease, N. Engl. J. Med., 368, 117, 10.1056/NEJMoa1211851 · DOI · Paper page
  36. Hamilton, 2020, The failure of microglia to digest developmental apoptotic cells contributes to the pathology of RNASET2-deficient leukoencephalopathy, Glia, 68, 1531, 10.1002/glia.23829 · DOI
  37. Hanamsagar, 2017, Generation of a microglial developmental index in mice and in humans reveals a sex difference in maturation and immune reactivity, Glia, 65, 1504, 10.1002/glia.23176 · DOI · Paper page
  38. Harrison, 2020, From polygenic scores to precision medicine in Alzheimer’s disease: a systematic review, J. Alzheimers Dis., 74, 1271, 10.3233/JAD-191233 · DOI
  39. Haud, 2011, rnaset2 mutant zebrafish model familial cystic leukoencephalopathy and reveal a role for RNase T2 in degrading ribosomal RNA, PNAS, 108, 1099, 10.1073/pnas.1009811107 · DOI
  40. Heckmann, 2020, Noncanonical function of an autophagy protein prevents spontaneous Alzheimer’s disease, Sci. Adv., 6
  41. Herradon, 2019, Connecting metainflammation and neuroinflammation through the PTN-MK-RPTPβ/ζ Axis: relevance in therapeutic development, Front. Pharmacol., 10
  42. Hornung, 2002, Quantitative expression of toll-like receptor 1–10 mRNA in cellular subsets of human peripheral blood mononuclear cells and sensitivity to CpG oligodeoxynucleotides, J. Immunol., 168, 4531, 10.4049/jimmunol.168.9.4531 · DOI
  43. Hu, 2001, Angiotensin-converting enzyme degrades Alzheimer amyloid β-Peptide (Aβ); retards aβ aggregation, deposition, Fibril Formation; and Inhibits Cytotoxicity. JBC, 276, 47863
  44. Javier-Torrent, 2019, Presenilin/γ-secretase-dependent epha3 processing mediates axon elongation through non-muscle myosin IIA, Elife, 8, 1, 10.7554/eLife.43646 · DOI
  45. Jehle, 2006, ATP-binding cassette transporter A7 enhances phagocytosis of apoptotic cells and associated ERK signaling in macrophages, J. Cell Biol., 174, 547, 10.1083/jcb.200601030 · DOI
  46. Johnson, 2020, Large-scale proteomic analysis of Alzheimer’s disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation, Nat. Med., 26, 769, 10.1038/s41591-020-0815-6 · DOI · Paper page
  47. Joshi, 2014, Microglia convert aggregated amyloid-β into neurotoxic forms through the shedding of microvesicles, Cell Death Differ., 21, 582, 10.1038/cdd.2013.180 · DOI
  48. Joshi, 2019, Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration, Nat. Neurosci., 22, 1635, 10.1038/s41593-019-0486-0 · DOI · Paper page
  49. Kader, 2017, MyD88-dependent inflammasome activation and autophagy inhibition contributes to Ehrlichia-induced liver injury and toxic shock, PLoS Pathog., 13, 10.1371/journal.ppat.1006644 · DOI
  50. Kanaan, 2021, Neuronal and glial distribution of tau protein in the adult rat and monkey, Front. Mol. Neurosci., 14, 10.3389/fnmol.2021.607303 · DOI · Paper page
  51. Kanatsu, 2016, Partial loss of CALM function reduces Aβ42 production and amyloid deposition in vivo, Hum. Mol. Genet., 25, 3988, 10.1093/hmg/ddw239 · DOI
  52. Karageorgos, 1997, Lysosomal biogenesis in lysosomal storage disorders, Exp. Cell Res., 234, 85, 10.1006/excr.1997.3581 · DOI
  53. Keren-Shaul, 2017, A unique microglia type associated with restricting development of Alzheimer’s disease, Cell, 169, 1276, 10.1016/j.cell.2017.05.018 · DOI · Paper page
  54. Köberlin, 2016, Functional crosstalk between membrane lipids and TLR biology, Curr. Opin. Cell Biol., 39, 28, 10.1016/j.ceb.2016.01.010 · DOI
  55. Kopec, 2018, Microglial dopamine receptor elimination defines sex-specific nucleus accumbens development and social behavior in adolescent rats, Nat. Commun., 9, 10.1038/s41467-018-06118-z · DOI
  56. La Rosa, 2017, Immune and imaging correlates of mild cognitive impairment conversion to Alzheimer’s disease, Sci. Rep., 7, 10.1038/s41598-017-16754-y · DOI
  57. Lambeth, 2019, Spontaneous isomerization of long-lived proteins providesa molecular mechanism for the lysosomal failure observed in Alzheimer’sDisease, ACS Cent. Sci., 5, 1387, 10.1021/acscentsci.9b00369 · DOI
  58. Langenfurth, 2014, Membrane-type 1 metalloproteinase is upregulated in microglia/brain macrophages in neurodegenerative and neuroinflammatory diseases, J. Neurosci. Res., 92, 275, 10.1002/jnr.23288 · DOI
  59. Lau, 2020, IL-33-PU.1 transcriptome reprogramming drives functional state transition and clearance activity of microglia in Alzheimer’s disease, Cell Rep., 31, 10.1016/j.celrep.2020.107530 · DOI · Paper page
  60. Ledo, 2020, Presenilin 1 phosphorylation regulates amyloid-beta degradation by microglia, Mol. Psychiatry
  61. Ledo, 2020, Lack of a site-specific phosphorylation of Presenilin 1 disrupts microglial gene networks and progenitors during development, PLoS One, 15, 10.1371/journal.pone.0237773 · DOI
  62. Lewandowska, 2004, Ultrastructural evaluation of activated forms of microglia in human brain in selected neurological diseases (SSPE, Wilson’s disease and Alzheimer’s disease), Folia Neuropathol., 42, 81
  63. Liao, 2010, Degradation of soluble and fibrillar amyloid β-Protein by matrix metalloproteinase (MT1-MMP) in vitro, Biochemistry, 49, 1127, 10.1021/bi901994d · DOI · Paper page
  64. Lotz, 2005, Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2 and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation in primary mouse microglial cell cultures, J. Neurochem., 94, 289, 10.1111/j.1471-4159.2005.03188.x · DOI
  65. Louvi, 2004, Presenilin 1 in migration and morphogenesis in the central nervous system, Development, 131, 3093, 10.1242/dev.01191 · DOI
  66. Mackay, 1997, A possible role for cathepsins d, e, and B in the processing of beta-amyloid precursor protein in Alzheimer’s disease, Eur. J. Biochem., 244, 414, 10.1111/j.1432-1033.1997.00414.x · DOI
  67. Majumdar, 2011, Degradation of Alzheimer’s amyloid fibrils by microglia requires delivery of ClC-7 to lysosomes, Mol. Biol. Cell, 22, 1664, 10.1091/mbc.e10-09-0745 · DOI
  68. Meng, 2020, Cholesterol handling in Lysosomes and beyond, Trends Cell Biol., 30, 452, 10.1016/j.tcb.2020.02.007 · DOI
  69. Mertins, 2017, An integrative framework reveals signaling-to-Transcription events in toll-like receptor signaling, Cell Rep., 19, 2853, 10.1016/j.celrep.2017.06.016 · DOI
  70. Miles, 2019, Small molecule binding to Alzheimer risk factor CD33 promotes aβ phagocytosis, ISCIENCE, 19, 110, 10.1016/j.isci.2019.07.023 · DOI
  71. Mueller-Steiner, 2006, Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer’s disease, Neuron, 51, 703, 10.1016/j.neuron.2006.07.027 · DOI
  72. Muth, 2019, Phagocytosis of apoptotic cells is specifically upregulated in ApoE4 expressing microglia in vitro, Front. Cell. Neurosci., 13, 181, 10.3389/fncel.2019.00181 · DOI
  73. Nakahira, 2011, Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome, Nat. Immunol., 12, 222, 10.1038/ni.1980 · DOI · Paper page
  74. Ni, 2019, Increased expression and altered subcellular distribution of cathepsin B in microglia induce cognitive impairment through oxidative stress and inflammatory response in mice, Aging Cell, 18
  75. Nicholson, 2016, Prosaposin is a regulator of progranulin levels and oligomerization, Nat. Commun., 7, 10.1038/ncomms11992 · DOI · Paper page
  76. Palmieri, 2011, Characterization of the CLEAR network reveals an integrated control of cellular clearance pathways, Hum. Mol. Genet., 20, 3852, 10.1093/hmg/ddr306 · DOI · Paper page
  77. Paolicelli, 2019, Cell-to-cell communication by extracellular vesicles: focus on microglia, Neuroscience, 405, 148, 10.1016/j.neuroscience.2018.04.003 · DOI · Paper page
  78. Park, 2011, Granulin is a soluble cofactor for toll-like receptor 9 signaling, Immunity, 34, 505, 10.1016/j.immuni.2011.01.018 · DOI
  79. Pizzo, 2020, Presenilin-2 and calcium handling: molecules, Organelles, cells and brain networks, Cells, 9, 1, 10.3390/cells9102166 · DOI
  80. Reddy, 2016, Dysregulation of nutrient sensing and CLEARance in presenilin deficiency, Cell Rep., 14, 2166, 10.1016/j.celrep.2016.02.006 · DOI
  81. Ristori, 2020, Amyloid-beta precursor protein APP down-regulation alters actin cytoskeleton-interacting proteins in endothelial cells, Cells, 9, 2506, 10.3390/cells9112506 · DOI
  82. Roach, 2005, The evolution of vertebrate Toll-like receptors, PNAS, 102, 9577, 10.1073/pnas.0502272102 · DOI
  83. Rogeberg, 2014, Identification of peptide products from enzymatic degradation of amyloid beta, Biochimie, 105, 216, 10.1016/j.biochi.2014.06.023 · DOI
  84. Roher, 1994, Proteolysis of aβ peptide from Alzheimer disease brain by Gelatinase A. Biochem, Biophys. Res. Commun., 205, 1755, 10.1006/bbrc.1994.2872 · DOI
  85. Rubio-Araiz, 2018, Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid, J. Neuroinflammation, 15, 247, 10.1186/s12974-018-1281-7 · DOI
  86. Rudnik, 2020, The lysosomal membrane - export of metabolites and beyond, FEBS J. febs.
  87. Sakae, 2019, Microglia in frontotemporal lobar degeneration with progranulin or C9ORF72 mutations, Ann. Clin. Transl. Neurol., 6, 1782, 10.1002/acn3.50875 · DOI
  88. Sannerud, 2016, Restricted location of PSEN2/γ-Secretase determines substrate specificity and generates an intracellular aβ pool, Cell, 166, 193, 10.1016/j.cell.2016.05.020 · DOI · Paper page
  89. Satoh, 2014, PLD3 is accumulated on neuritic plaques in Alzheimer’s disease brains, Alzheimers Res. Ther., 6, 70, 10.1186/s13195-014-0070-5 · DOI
  90. Schmechel, 1993, Increased amyloid β-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease, PNAS U. S. A., 90, 9649, 10.1073/pnas.90.20.9649 · DOI · Paper page
  91. Scholtzova, 2009, Induction of toll-like receptor 9 signaling as a method for ameliorating Alzheimer’s disease-related pathology, J. Neurosci., 29, 1846, 10.1523/JNEUROSCI.5715-08.2009 · DOI · Paper page
  92. Scholtzova, 2014, Amyloid β and Tau Alzheimer’s disease related pathology is reduced by Toll-like receptor 9 stimulation, Acta Neuropathol. Commun., 2, 101
  93. Scholtzova, 2017, Innate immunity stimulation via toll-like receptor 9 ameliorates vascular amyloid pathology in Tg-SwDI mice with associated cognitive benefits, J. Neurosci., 37, 936, 10.1523/JNEUROSCI.1967-16.2016 · DOI · Paper page
  94. Solé-Domènech, 2018, Lysosomal enzyme tripeptidyl peptidase 1 destabilizes fibrillar Aβ by multiple endoproteolytic cleavages within the β-sheet domain, PNAS, 115, 1493, 10.1073/pnas.1719808115 · DOI
  95. Stancu, 2019, Aggregated Tau activates NLRP3-ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo, Acta Neuropathol., 137, 599, 10.1007/s00401-018-01957-y · DOI · Paper page
  96. Stoka, 2016, Lysosomal cathepsins and their regulation in aging and neurodegeneration, Ageing Res. Rev., 32, 22, 10.1016/j.arr.2016.04.010 · DOI · Paper page
  97. Storck, 2018, The concerted amyloid-beta clearance of LRP1 and ABCB1/P-gp across the blood-brain barrier is linked by PICALM, Brain Behav. Immun., 10.1016/j.bbi.2018.07.017 · DOI · Paper page
  98. Strickland, 2019, Dr. Jekyll and Mr. Hyde: ApoE explains opposing effects of neuronal LRP1, J. Clin. Invest., 129, 969, 10.1172/JCI127578 · DOI · Paper page
  99. Swanson, 2020, Identification of a dysfunctional microglial population in human Alzheimer’s disease cortex using novel single-cell histology image analysis, Acta Neuropathol. Commun., 8, 170, 10.1186/s40478-020-01047-9 · DOI
  100. Szepesi, 2018, Bidirectional microglia–Neuron communication in health and disease, Front. Cell. Neurosci., 12, 1, 10.3389/fncel.2018.00323 · DOI · Paper page
  101. Tahara, 2006, Role of toll-like receptor signalling in A uptake and clearance, Brain, 129, 3006, 10.1093/brain/awl249 · DOI · Paper page
  102. Takahashi, 2017, Opposing effects of progranulin deficiency on amyloid and tau pathologies via microglial TYROBP network, Acta Neuropathol., 133, 785, 10.1007/s00401-017-1668-z · DOI
  103. Tucker, 2000, The plasmin system is induced by and degrades Amyloid-β aggregates, J. Neurosci., 20, 3937, 10.1523/JNEUROSCI.20-11-03937.2000 · DOI
  104. Ubelmann, 2017, Bin1 and CD2AP polarise the endocytic generation of beta-amyloid, EMBO Rep., 18, 102, 10.15252/embr.201642738 · DOI · Paper page
  105. Van Acker, 2019, Connecting the dots in the neuroglobin-protein interaction network of an unstressed and ferroptotic cell death neuroblastoma model, Cells, 8, 873, 10.3390/cells8080873 · DOI
  106. Van Gool, 2019, LRP1 has a predominant role in production over clearance of aβ in a mouse model of Alzheimer’s disease, Mol. Neurobiol., 56, 7234, 10.1007/s12035-019-1594-2 · DOI · Paper page
  107. van Niel, 2018, Shedding light on the cell biology of extracellular vesicles, Nat. Rev. Mol. Cell Biol., 19, 213, 10.1038/nrm.2017.125 · DOI · Paper page
  108. Venegas, 2017, Microglia-derived ASC specks cross-seed amyloid-β in Alzheimer’s disease, Nature, 552, 355, 10.1038/nature25158 · DOI · Paper page
  109. Villa, 2018, Sex-specific features of microglia from adult mice, Cell Rep., 23, 3501, 10.1016/j.celrep.2018.05.048 · DOI · Paper page
  110. Von Bernhardi, 2015, Microglial cell dysregulation in brain aging and neurodegeneration, Front. Aging Neurosci., 20, 124
  111. Walker, 2018, Increased expression of toll-like receptor 3, an anti-viral signaling molecule, and related genes in Alzheimer’s disease brains, Exp. Neurol., 309, 91, 10.1016/j.expneurol.2018.07.016 · DOI
  112. Williamson, 2017, Disruption of amyloid precursor protein ubiquitination selectively increases amyloid (A) 40 levels via presenilin 2-mediated cleavage, JBC, 292, 19873, 10.1074/jbc.M117.818138 · DOI
  113. Wingo, 2021, Integrating human brain proteomes with genome-wide association data implicates new proteins in Alzheimer’s disease pathogenesis, Nat. Genet., 53, 143, 10.1038/s41588-020-00773-z · DOI · Paper page
  114. Wu, 2019, Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy, Cell Rep., 28, 2111, 10.1016/j.celrep.2019.07.060 · DOI · Paper page
  115. Wyatt-Johnson, 2020, The complexity of microglial interactions with innate and adaptive immune cells in Alzheimer’s disease, Front. Aging Neurosci., 12, 10.3389/fnagi.2020.592359 · DOI · Paper page
  116. Xu, 2020, TFEB regulates lysosomal exocytosis of tau and its loss of function exacerbates tau pathology and spreading, Mol. Psychiatry, 1
  117. Yambire, 2019, Impaired lysosomal acidification triggers iron deficiency and inflammation in vivo, Elife, 8, 10.7554/eLife.51031 · DOI
  118. Yan, 2006, Matrix Metalloproteinase-9 degrades Amyloid-β fibrils in vitro and compact plaques in situ, JBC, 281, 24566, 10.1074/jbc.M602440200 · DOI · Paper page
  119. Yang, 2021, Genomic atlas of the proteome from brain, CSF and plasma prioritizes proteins implicated in neurological disorders, Nat. Neurosci., 10.1038/s41593-021-00886-6 · DOI · Paper page
  120. Yanguas-Casás, 2020, Aging and sex: impact on microglia phagocytosis, Aging Cell, 19, 10.1111/acel.13182 · DOI · Paper page
  121. Yao, 2019, Pseudoginsenoside‐F11 alleviates oligomeric β‐amyloid‐induced endosome‐lysosome defects in microglia, Traffic, 20, 61, 10.1111/tra.12620 · DOI

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Metadata

Authors
Van Acker, Z. P., Perdok, A., Bretou, M., & Annaert, W.
ORCID
Venue
Ageing Research Reviews
Publisher
Elsevier BV
Published
2021-11
Volume
71
Pages
101444
ISSN
1568-1637
DOI
10.1016/j.arr.2021.101444
Cited by
45
References
43
Language
en
Licence
Funders
  • Vlaams Instituut voor Biotechnologie
  • Alzheimer's Association (1S35019N, AARF-18-564825, AARF-20-677499)
  • Fonds Wetenschappelijk Onderzoek (12ZL321N, G056017 N, G078117 N, G0C4220 N, S006617 N)
  • KU Leuven (C14/21/095, C15/15/073)

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