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Choy, T.

Publications and source records attributed to Choy, T..

2 recordsLinked to original sources

Spontaneous reinstatement of episodic memories in the developing human brain

Starting early in development, the hippocampus can support the formation of episodic memories, and yet how the developing brain stabilizes these memories to support their long-term accessibility has not been established. This study (N = 49; mean age = 11.68 years) examined how encoded episodic memories are stabilized in development. Using fMRI and multivariate analyses, we tracked neural reinstatement of newly learned item-location-context associations in youth. During encoding, hippocampus and visual cortex activity predicted later memory success. Crucially, during post-encoding rest, spontaneous pattern reinstatement in the angular gyrus and the pregenual medial prefrontal cortex (mPFC) also predicted memory, with age-related changes in the mPFC and superior frontal gyrus. These findings suggest that episodic memory stabilization during childhood and adolescence is broadly supported by developmental change within regions associated with mature function, advancing our understanding of how different memory stages contribute to how we learn and remember across the lifespan.

neuroscience↗

Astrocytic Slc4a4 regulates blood-brain barrier integrity in healthy and stroke brains via a NO-CCL2-CCR2 pathway

Astrocytes play vital roles in blood-brain barrier (BBB) maintenance, yet how they support BBB integrity under normal or pathological conditions remains poorly defined. Recent evidence suggests pH homeostasis is a new cellular mechanism important for BBB integrity. In the current study, we investigated the function of an astrocyte-specific pH regulator, Slc4a4, in BBB maintenance and repair. We show that astrocytic Slc4a4 is required for normal astrocyte morphological complexity and BBB function. Multi-omics analyses identified increased astrocytic secretion of CCL2 coupled with dysregulated arginine-NO metabolism after Slc4a4 deletion. Using a model of ischemic stroke, we found that loss of Slc4a4 exacerbates BBB disruption and reactive gliosis, which were both rescued by pharmacological or genetic inhibition of the NO-CCL2 pathway in vivo. Together, our study identifies the astrocytic Slc4a4-NO-CCL2 axis as a pivotal mechanism controlling BBB integrity and repair, while providing insights for a novel therapeutic approach against BBB-related CNS disorders.

neuroscience↗