Cover Illustration: Confocal microscopy image of glutamate aspartate transporters (GLAST) on Bergmann glia closely ensheathing Purkinje neuron dendrites in the mouse cerebellar cortex (blue, DAPI; green, GLAST; magenta, calbindin). Bergmann glia are specialized radial astrocytes that rely on nitric oxide production to effectively interact with Purkinje neurons. (See Tellios, V., et al, https://doi.org/10.1002/glia.24143.)

• Monocytes support remyelination, yet differential contribution of subsets is unknown.
• Monocyte dysregulation with ageing and disease may cause remyelination failure.
• Targeting monocytes is a promising strategy to promote remyelination.

• Pioneer Cajal studies claimed for morphological (and likely functional) heterogeneity of astrocytes.
• Neuron-Astrocyte interaction challenged the view of the SCN circuit.
• Circadian properties of astrocytes and key role in time-keeping.

• Early-life malnutrition and specific gut microbes shape cognition and microglia in mice.
• Altered microglial features occur independently from significant neuroinflammation or BBB deficits, but were linked to impaired lipid metabolism.
• PAO diet (ω3 PUFA/antioxidant-associated supplement) improves cognitive features of malnutrition.

• Astrocytes are effective target cells for gene therapy against amyotrophic lateral sclerosis.
• SOD1-targeting gene therapy in astrocytes protects fast-fatigable motor units.
• RNAi gene therapy directed to astrocytes induces motoneuron plasticity.

• nNOS^-/- BG exhibited reduced GLAST function with D-aspartate simulation compared to WT BG.
• nNOS^-/- BG in vivo displayed less Purkinje neuron ensheathment compared to WT BG.
• Supplementation of exogenous NO increased GLAST plasma membrane expression in nNOS^-/- BG in ex vivo and in vitro culture conditions.

• Lgals3 is upregulated in monocyte/macrophage populations.
• Galectin-3/MAC2 labels bone marrow-derived monocytes 6–10 months following cell infiltration into the CNS, but not microglia.
• MAC2 is not a specific marker for plaque-associated microglia.

• Cerebral ischemia triggers astrocytic p75^NTR upregulation, promoting neuroinflammation via NF-κB and HIF-1α pathways to increase BBB disruption.
• Genetic/pharmacological inhibition of p75^NTR ameliorates ischemic brain injury including BBB damage.

• Age- and LPS-specific mRNA profiles were evident in glia.
• Aging-associated microglial reactivity to LPS challenge was paralleled by astrocyte immunosenescence.
• Astrocytic IL-10R^KO induced an “aged” neuroinflammatory response to LPS challenge.

• Striatal injection of synuclein fibrils in mice to model PD.
• No correlation between inclusions, neurodegeneration, microgliosis.
• Transcriptomics reveals microglia response preceding neurodegeneration.
• Molecular pathways overlap with those of PD.

• Potassium efflux through postsynaptic NMDA receptors depolarizes perisynaptic astroglia.
• Potassium-mediated depolarization reduces astrocytic glutamate uptake.
• Reduced uptake boosts glutamate spillover actions.

• Long-term intravital imaging revealed a fibrous collagen-rich scar formation in the microinfarct with accumulation of GFAP+ reactive astrocytes, transient BBB dysfunction with impaired pericyte-vessel coverage and neuronal loss.

• GATA6 is upregulated in SMA astrocytes and is associated with increased glial activation, enhanced pro-inflammatory ligand production, altered microglial morphology and phagocytosis, and motor neuron toxicity.