Dear Colleagues,

Microglia colonize the CNS in early embryogenesis and are established by birth as an autonomously maintained population for the lifetime of the host. These glial cells fulfil tissue homeostasis functions and recently there has been an explosion in new findings giving us insight into the involvement of microglia in CNS disorders. A host of new molecular tools and mouse models of disease are increasingly implicating microglia as a key player in conditions ranging from neurodevelopmental disorders, expressing functional phenotypes sculpting developing neuronal circuits and guiding learning-associated plasticity; to neuroinflammatory and neurodegenerative disorders, where microglia progressively change their functional capability. Although much still needs to be learned, the emerging picture is that microglia can be both protective and detrimental, and understanding the physiological functions of these cells is crucial to determining their roles in disease.

The goal of this Special Issue is to provide a panorama of the ongoing efforts in elucidating the functions of microglia in neurological disease. We aim to cover a wide range of pathologies, including developmental pathologies and those ranging from traumatic to classically inflammatory and degenerative.

We look forward to your contributions.

Prof. Dr. Kate Lykke Lambertsen
Prof. Dr. Bente Finsen
Guest Editors

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Title: Microglia-derived extracellular vesicles enhance oligodendro-cyte maturation by transcriptionally regulating mitochondrial molecular pathways
Authors: Stefano Raffaele 1, Marta Lombardi 2, Claudia Verderio 2 and Marta Fumagalli 1,*
Affiliation: 1 Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20133 Milan, Italy 2 CNR Institute of Neuroscience, Vedano al Lambro, MB, 20854, Italy
Abstract: Abstract (Max 200 words): Degeneration of myelinating oligodendrocytes (OLs) and consequent disruption of the myelin sheath enwrapping neuronal axons represent major contributing factors to neurodegeneration and disability in several neuropathological conditions. Fostering endog-enous myelin repair sustained by oligodendrocyte precursor cells (OPCs) is therefore considered a promising therapeutic approach to preserve neuronal integrity and to counteract disease pro-gression. A central role in shaping remyelination is played by microglia, that influence both myelin damage and repair processes by acquiring different functional states. In this respect, ex-tracellular vesicles (EVs) released by microglia emerged as pivotal players in the communication with OPCs. Our recent studies show that EVs derived from pro-regenerative microglia efficiently enhanced OPC maturation and remyelination in different experimental settings. However, the mechanisms underlying EV-induced beneficial effects on OPCs still need to be elucidated. Here, we performed a transcriptomic profiling of primary OPCs exposed to either pro-inflammatory (i-EVs) or pro-regenerative (IL4-EVs and MSC-EVs) microglial EVs, revealing prominent changes induced by protective types of EVs compared to untreated cells (CTRL), while i-EVs were less potent. Bi-oinformatic tools have been exploited to identify the molecular pathways significantly modulated by EVs in recipient OPCs, showing that most of them were in common between IL4-EVs and MSC-EVs, and to predict the upstream regulators that might be responsible for these transcrip-tional changes. Results suggest that rewiring of mitochondria-associated molecular pathways in OPCs underpins the pro-differentiating action of microglial EVs, opening novel perspectives for remyelinating therapies.

Title: 18 kDa Translocator Protein is required to ensure cholesterol homeostasis in activated human microglia avoiding the acquisition of exaggerated pro-inflammatory phenotype
Authors: Elisa Angeloni1, Lorenzo Germelli1, Laura Marchetti1,2, Eleonora Da Pozzo*1,2, Christian H Wetzel3, Federico Da Settimo1, Maria Letizia Trincavelli1, Claudia Martini1, Barbara Costa1,2
Affiliation: 1Department of Pharmacy, University of Pisa, via Bonanno 6, 56126 Pisa, Italy. 2Center for Instrument Sharing University of Pisa (CISUP), Lungarno Pacinotti, 43/44 – 56126 Pisa, Italy. 3Department of Psychiatry and Psychotherapy, Molecular Neurosciences, University of Regensburg, 93059 Regensburg, Germany.