Vanishing White Matter Disease mutations compromise the function of the essential translation initiation factor eIF2B by destabilizing the holoenzyme, and the small molecule ISRIB reverses their pathogenic effect by promoting complex formation.

A cell-cell contact between microglial SIRPα and CD47 on neighboring cells is a critical module for phase conversion of microglia in the brain white matter and controls demyelination.

A subcortical white matter connection from the pulvinar to the amygdala predicts how well we recognise fearful faces and the strength of feed-forward neural connectivity.

Oligodendrocytes in white matter use Kir4.1 inwardly rectifying potassium channels to prevent extracellular potassium accumulation, enabling neurons to sustain repetitive firing and limiting the initiation of seizures.

Primate attention is not limited to a dorsal fronto-parietal network, but includes a ventral temporal node and its dorso-ventral interactions with other attentional areas.

ATP imaging of spiking optic nerve axons in real time reveals correlation between ATP levels and electrical activity as well as contribution of lactate metabolism to axonal ATP homeostasis.

The amyloid patterns overlap with the default-mode network, whereas the tau patterns overlap with distinct functional networks and are associated with a loss of anatomical connectivity and multiple cognitive functions.

Although central nervous system (CNS) regeneration has been considered to be controlled by CNS microenvironment, CNS injury causes leading to leakage of circulating factors into CNS, which promotes CNS regeneration.

Ultrastructural and loss-of-function experiments show that oligodendrocyte-encoded Kir4.1 is located near active axonal structures, including within myelin inner tongue, and has critical functions to promote axonal activity and preserve integrity.

High-level disorders, such as motor awareness, are not localised in the brain but emerge from the interaction between brain circuits.