After many years of being largely neglected in neurodegenerative disease, the past few years have seen a turning point in the field’s view on the impact of microglia in neurological disorders. 2018 has been another exciting year with a number of great contributions in this area.
Key advances
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LRRC33 regulates the local activation and release of TGFβ1 in the CNS.
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Senescent microglia and astroglia drive tau phosphorylation and neurofibrillary tangle formation in a non-cell autonomous manner.
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Mononuclear phagocytes dynamically adapt their phenotype based on astroglial signals.
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Microglial cell renewal following CSF1R1 inhibition depends on proliferation of surviving CNS-resident microglia.
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Microglia are involved in TDP43 clearance from neurons and promote recovery from motor symptoms in a mouse model of ALS.
References
Qin, Y. et al. A milieu molecule for TGFβ required for microglia function in the nervous system. Cell 174, 156–171 (2018).
Bussian, T. J. et al. Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline. Nature 562, 578–582 (2018).
Brelstaff, J. et al. Living neurons with tau filaments aberrantly expose phosphatidylserine and are phagocytosed by microglia. Cell Rep. 24, 1939–1948 (2018).
Locatelli, G. et al. Mononuclear phagocytes locally specify and adapt their phenotype in a multiple sclerosis model. Nat. Neurosci. 21, 1196–1208 (2018).
Huang, Y. et al. Repopulated microglia are solely derived from the proliferation of residual microglia after acute depletion. Nat. Neurosci. 21, 530–540 (2018).
Spiller, K. J. et al. Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy. Nat. Neurosci. 21, 329–340 (2018).
Acknowledgements
M.T.H. is supported by grants from the Deutsche Forschungsgesellschaft (SFB 1089, excellence cluster ImmunoSensation) and by the European Union Joint Programme–Neurodegenerative Disease (JPND) consortium InCure (funding code 01ED1505A).
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Heneka, M.T. Microglia take centre stage in neurodegenerative disease. Nat Rev Immunol 19, 79–80 (2019). https://doi.org/10.1038/s41577-018-0112-5
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DOI: https://doi.org/10.1038/s41577-018-0112-5
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