• Many processes localized in astroglia are potentially neuroprotective
• In this review we examine how astroglial dysfunction contributes to neurodegeneration and major neurological disorders and explore potential drug targets localized to astrocytes.

Astrocytes display morphological and functional atrophy in patients with depression.

Dysfunctional astrocytes lead to depressive-like phenotypes.

Antidepressant treatments may exert their therapeutic effects on astrocytes.

• Microglia uptakes MPP⁺ through OCT3.
• MPP⁺ specifically potentiates the production of TNF-α in microglia through downregulation of miR-7116-5p, contributing to exacerbated inflammation expression and DA damage.

• In HIV infection, decreased brain HO-1 protein expression accompanies increased HO-1 RNA and immunoproteasome expression
• In astrocytes IFNγ increases immunoproteasome subunit expression and proteasome-dependent HO-1 protein degradation

• Human SCs exhibit a safe therapeutic profile with an absence of tumorigenicity long-term in a xenotransplant paradigm of contusive SCI
• Introduction of human SCs into the injured cord produced an environment conducive to cyst reduction, enhanced white matter preservation, axon growth and myelination

• Tau oligomers enter astrocytes more efficiently than neurons.
• Tau treatment affects Ca²⁺-dependent gliotransmitter release.
• Tau induces ATP-dependent inhibition of synaptic protein expression and synaptic transmission.

1. Oligodendrocyte susceptibility to early postnatal EtOH exposure indicates heterogeneity based on ontogenetic origin.
2. Despite the recovery of acute oligodendrocyte losses by adulthood, MBP dysregulation and WM microstructural abnormalities persist.

• Retinal damage/degeneration models were developed in Xenopus.
• They allowed revealing that Müller cells actively re-enter the cell cycle upon injury and contribute to photoreceptor cell replacement in Xenopus laevis.

• In multiple sclerosis lesions (MS) and distinct experimental models of de- and remyelination, we observed efficient remyelination of damaged axons, suggesting axon protection by remyelination both in early and late stage lesions.

• TGF-βs are required for 4AP-dependent NBCe1 activation
• 4AP activates TGF-βs
• Activation of TGF-β signaling up-regulates transcript, protein and functional expression of NBCe1
• TGF-βs regulate transcriptional expression of NBCe1 through Smad4

• The novel steroid derivative BNN27 protects OLs from apoptosis when they are challenged in vitro with the cuprizone toxin, in a TrkA-dependent manner.
• In addition, BNN27 regulates OLs during demyelination in vivo and reduces microgliosis.