In an empty microglial niche, repopulating microglia arise from subventricular zone and white matter-associated areas without contributions from the bone marrow to fill the mouse brain via a spreading wave.
Neurological pathology and chronic activation of the induced stress response are caused by expression of a truncated EIF2B5 in vanishing white matter disease.
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.
White matter microstructure alterations in key bundles affected in Alzheimer's disease are related to amyloid and tau pathology in the preclinical phase of sporadic and autosomal-dominant Alzheimer's disease.
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.
In silico modelling of all available data shows that a twenty-day ascending-dose primaquine regimen could be safe to administer to G6PD deficient patients for the radical cure of vivax malaria.
