Erik Nutma

196 Chapter 8 Disease. Immunity. Jan 14 2020;52(1):167-182 e7. doi:10.1016/j.immuni.2019.12.004 85. Baker D, et al. Both cladribine and alemtuzumab may effect MS via B-cell depletion. NeurologyNeuroimmunology Neuroinflammation. 2017;4(4) 86. Gelfand JM, et al. Ocrelizumab and Other CD20(+) B-Cell-Depleting Therapies in Multiple Sclerosis. Neurotherapeutics. Oct 2017;14(4):835-841. doi:10.1007/s13311-017-0557-4 87. Li R, et al. Reassessing B cell contributions inmultiple sclerosis. Nat Immunol. Jul 2018;19(7):696-707. doi:10.1038/s41590-018-0135-x 88. Greenfield AL, et al. B-cell Therapy for Multiple Sclerosis: Entering an era. Ann Neurol. Jan 2018;83(1):13-26. doi:10.1002/ana.25119 89. Schirmer L, et al. Neuronal vulnerability and multilineage diversity in multiple sclerosis. Nature. Sep 2019;573(7772):75-82. doi:10.1038/s41586019-1404-z 90. Absinta M, et al. A lymphocyte-microglia-astrocyte axis in chronic active multiple sclerosis. Nature. Sep 2021;597(7878):709-714. doi:10.1038/s41586021-03892-7 91. MiedemaA, etal.Brainmacrophagesacquiredistinct transcriptomes prior to demyelination in multiple sclerosis. bioRxiv. 2021:2021.10.27.465877. doi:10.1101/2021.10.27.465877 92. Fonseca MI, et al. Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain. J Neuroinflammation. Mar 6 2017;14(1):48. doi:10.1186/s12974-017-0814-9 93. Stephan AH, et al. A dramatic increase of C1q protein in the CNS during normal aging. J Neurosci. Aug 14 2013;33(33):13460-74. doi:10.1523/ JNEUROSCI.1333-13.2013 94. Peferoen LA, et al. Activation status of human microglia is dependent on lesion formation stage and remyelination in multiple sclerosis. J Neuropathol Exp Neurol. Jan 2015;74(1):48-63. doi:10.1097/NEN.0000000000000149 95. van Wageningen TA, et al. Regulation of microglial TMEM119 and P2RY12 immunoreactivity in multiple sclerosis white and grey matter lesions is dependent on their inflammatory environment. Acta Neuropathol Commun. Dec 11 2019;7(1):206. doi:10.1186/s40478-019-0850-z 96. van Horssen J, et al. Clusters of activated microglia in normal-appearing white matter show signs of innate immune activation. Journal of neuroinflammation. 2012;9(1):1-9. 97. Allen SJ, et al. Isolation and characterization of cells infiltrating the spinal cord during the course of chronic relapsing experimental allergic encephalomyelitis in the Biozzi AB/H mouse. Cell Immunol. Feb 1993;146(2):335-50. doi:10.1006/ cimm.1993.1031 98. Bauer J, et al. The role of macrophage subpopulations in autoimmune disease of the central nervous system. Histochem J. Feb 1996;28(2):83-97. doi:10.1007/BF02331413 99. Trebst C, et al. Update on the diagnosis and treatment of neuromyelitis optica: recommendations of the Neuromyelitis Optica Study Group (NEMOS). J Neurol. Jan 2014;261(1):116. doi:10.1007/s00415-013-7169-7 100.Wlodarczyk A, et al. Type I interferon-activated microglia are critical for neuromyelitis optica pathology. Glia. Apr 2021;69(4):943-953. doi:10.1002/glia.23938 101. van der Knaap MS, et al. Leukodystrophies: a proposedclassificationsystembasedonpathological changes and pathogenetic mechanisms. Acta Neuropathol. Sep 2017;134(3):351-382. doi:10.1007/s00401-017-1739-1 102. Adams SJ, et al. Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP): Integrating the literature on hereditary diffuse leukoencephalopathy with spheroids (HDLS) and pigmentary orthochromatic leukodystrophy (POLD). J Clin Neurosci. Feb 2018;48:42-49. doi:10.1016/j.jocn.2017.10.060 103.Oyanagi K, et al. Adult onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and Nasu-Hakola disease: lesion staging and dynamic changes of axons and microglial subsets. Brain Pathol. Nov 2017;27(6):748-769. doi:10.1111/bpa.12443 104. Dai XM, et al. Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte deficiency, increased primitive progenitor cell frequencies, and reproductive defects. Blood. Jan 1 2002;99(1):11120. doi:10.1182/blood.v99.1.111 105. Erblich B, et al. Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits. PLOS ONE. 2011;6(10):e26317. doi:10.1371/ journal.pone.0026317 106.Oosterhof N, et al. Colony-Stimulating Factor 1 Receptor (CSF1R) Regulates Microglia Density and Distribution, but Not Microglia Differentiation In Vivo. Cell Rep. Jul 31 2018;24(5):1203-1217 e6. doi:10.1016/j.celrep.2018.06.113 107. Kempthorne L, et al. Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy. Acta Neuropathol Commun. May 19 2020;8(1):72. doi:10.1186/s40478-020-00947-0 108. Hakola HP, et al. Osteodysplasia polycystica hereditaria combined with sclerosing leucoencephalopathy, a new entity of the dementia praesenilis group. Acta Neurol Scand. 1970;46(S43):79-80. 109. Hakola HPA. Neuropsychiatric and genetic aspects of a new herediary disease characterized by progressive dementia and lipomembranous polycytic osteodysplasia. Acta Psychiatr Scand Suppl. 1972;232:1-173. 110.Nasu T, et al. A lipid metabolic disease—

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