News & Comment

Elevated maternal IL-6 in the maternal circulation can enter the fetus via the maternal—placental—fetal route and alter neurodevelopmental processes, with potentially wide-ranging effects on brain function later in life.

A new study suggests an evolutionary mechanism — involving abnormal spindle-like microcephaly-associated protein — that, in part, underlies cerebral cortical expansion.

Different 3′ untranslated regions of mRNA transcripts are associated with differences in mRNA localization, translation, stability and activity-dependent changes in expression.

In the mouse postnatal hippocampus, microglia trim presynaptic structures by a partial phagocytic process termed trogocytosis and remodel postsynaptic structures.

Distinct output pathways of the nucleus accumbens mediate the opposing effects of context on relapse to alcohol seeking.

Brain implants are being trialled for their potential to ameliorate treatment-resistant conditions or to restore function. However, there are no clear guidelines for continued access to brain implants for trial participants whose symptoms improve with these devices.

In mice, aggression is regulated by the circadian suprachiasmatic nucleus through at least two neural pathways.

A combination of electrochemical neuromodulation of spinal leg circuits and physical training in a robotic rehabilitation system restored volitional locomotion in rodents with severe spinal cord injury.

Two studies provide insight into the neural circuits integrating competing threat signals, such as pain and hunger.

A study of post-mortem brains from individuals of difference ages suggests that hippocampal neurogenesis in humans decreases during childhood and is absent in adults.

In the spinal cord and thalamus of mice, astrocyte-generated interleukin-33 instructs microglia to engulf synapses and thus regulates neural circuit development.

This study shows that human neural stem cell grafts re-establish a neuronal relay across spinal cord injury in rhesus monkeys.

Study employs DNA methylation editing to reactivateFMR1expression and reverse phenotypic deficits in cells derived from individuals with fragile X syndrome.