A NPAS4-NuA4 complex couples synaptic activity to DNA repair.

Neuronal activity is crucial for adaptive circuit remodelling but poses an inherent risk to the stability of the genome across the long lifespan of postmitotic neurons. Whether neurons have acquired specialized genome protection mechanisms that enable them to withstand decades of potentially damaging stimuli during periods of heightened activity is unknown. Here we identify an activity-dependent DNA repair mechanism in which a new form of the NuA4-TIP60 chromatin modifier assembles in activated neurons around the inducible, neuronal-specific transcription factor NPAS4.

The CD24 surface antigen in neural development and disease.

A cell's surface molecular signature enables its reciprocal interactions with the associated microenvironments in development, tissue homeostasis and pathological processes. The CD24 surface antigen (heat-stable antigen, nectadrin; small cell lung cancer antigen cluster-4) represents a prime example of a neural surface molecule that has long been known, but whose diverse molecular functions in intercellular communication we have only begun to unravel. Here, we briefly summarize the molecular fundamentals of CD24 structure and provide a comprehensive review of CD24 expression and functional studies in mammalian neural developmental systems and disease models (rodent, human).

Obesity Weighs down Memory through a Mechanism Involving the Neuroepigenetic Dysregulation of Sirt1.

Unlabelled: Aberrant gene expression within the hippocampus has recently been implicated in the pathogenesis of obesity-induced memory impairment. Whether a dysregulation of epigenetic modifications mediates this disruption in gene transcription has yet to be established. Here we report evidence of obesity-induced alterations in DNA methylation of memory-associated genes, including Sirtuin 1 (Sirt1), within the hippocampus, and thus offer a novel mechanism by which SIRT1 expression within the hippocampus is suppressed during obesity.