Violations of strong memory-based predictions trigger a cascade of changes in cognitive control, attention, and arousal, with differential impacts on the encoding of unexpected information into memory.
Human forebrain organoids reveal that amyloid-driven microglia recruit killer T cells via CCL5, forming a self-amplifying neuroinflammatory loop targetable by CCR5 or CXCR3 blockade.
In mammalian neocortex, opposing Krüppel-like factor (KLF) transcription factors first activate and then repress a genetic program related to axon outgrowth, potentially contributing to loss of cortical axon outgrowth in the adult.
Genetic lineage tracing and live-cell imaging demonstrate that NeuroD1 does not convert microglia into neurons but instead promotes microglial apoptosis, challenging claims of in situ glia-to-neuron conversion.
