José P. López‐Atalaya

The paper identifies molecular and functional differences between suprapyramidal and infrapyramidal blades in the mouse dentate gyrus using multi-omics approaches.

The paper investigates metabolic and transcriptional changes in microglia after phagocytosis, showing these adaptations sustain their functionality and regenerative properties.

The paper identifies CD74+ microglia/macrophages driven by MIF as clinically relevant subpopulations in brain metastasis and other CNS disorders, showing their role in disease progression and therapeutic targeting potential.

This study identifies sex-dependent interferon signaling as a driver of female-biased Alzheimer's disease vulnerability, showing that targeting this pathway can reduce pathology and improve cognition in female mice.

The paper generates a single-cell multiomic atlas of the embryonic mouse thalamus, identifies two major glutamatergic lineages, and reveals early lineage divergence that segregates sensory and non-sensory circuits.

This study shows that a single cocaine exposure causes long-lasting 3D genome structure changes in midbrain dopamine neurons, affecting gene regulation and synaptic plasticity.

This study shows that SFRP1 from astrocytes promotes microglial activation in acute and chronic neuroinflammation, suggesting it as a therapeutic target.

The paper identifies sublayer- and cell-type-specific transcriptional changes in hippocampal sclerosis using single-nucleus and bulk RNA sequencing, revealing distinct neurodegenerative trajectories in superficial CA1 neurons.

The paper shows neurons and astrocytes in specific brain regions share transcriptional and epigenetic signatures, which are maintained even after reprogramming.

The paper identifies an alternative Wnt signaling pathway regulated by Zic2 that mediates axon repulsion by modulating β-catenin phosphorylation and Eph signaling.

The paper shows that MIR3607 promotes cerebral cortex expansion by activating Wnt/βCatenin signaling in mouse embryos and human organoids.