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When oligodendrocytes lack expression of the low-abundant myelin protein CMTM5, central nervous system axons are myelinated normally but subsequently degenerate involving a Wallerian-like pathomechanism.

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.

MMnet is a conserved, trans-regulated gene network that controls skeletal homeostasis through osteoclast multinucleation and bone resorptive function.

An individualized cross-frequency coupling approach identified slow oscillation-spindle coupling strength as a novel mechanism that mediates memory formation during cortical maturation.

New evidence of brain proinflammatory cascades supports post-acute sequelae of SARS-CoV-2 infection, ultimately promoting the onset and progression of Alzheimer's disease as a function of age.

Molecular genetics identifies a novel microglial pathway essential for mouse brain development and a previously unknown anti-inflammatory activity of monomeric amyloid β that activates this pathway.

Preventing activity of the kinase tumor progression locus 2 modulates microglial activation, reduces T-cell brain infiltration, and is neuroprotective in disease models.

The Zip3-like protein Vilya links the initiation of meiotic recombination with crossover formation.

Based on benchmarking various methods and analyzing multiple real scRNA-seq datasets, a computational platform/workflow and a set of tips for best practices are developed for analyzing causal interactions or relationships in single cells.