Sleep is known to contribute to the healthy functioning of the brain and the consolidation of memories. Past psychology research specifically highlighted its role in retaining episodic memories, which are memories of specific events or experiences.

Researchers at Rotman Research Institute at Baycrest Academy for Research and Education, University of Toronto and other institutes recently carried out a study to better understand the extent to which sleep transforms how we remember real-world experiences over time and what processes could underpin this transformation. Their findings, published in Nature Human Behaviour, suggest that sleep actively and selectively improves the accuracy with which we remember one-time real-world experiences.

“My lab studies real-life memory such as the memory of events that occur as part of daily experiences,” Brian Levine, senior author of the paper, told Medical Xpress. “We are interested in how these memories are transformed over time and why some elements are remembered while others are forgotten. This is hard to do with naturalistic events in peoples’ lives where we have no control over what happened. So we set up the Baycrest Tour as a controlled but naturalistic event that we could use to test memory.”

A new imaging technique is helping ultra-powerful MRI scanners detect tiny differences in the brains of patients with treatment-resistant epilepsy. In a groundbreaking study, doctors at Addenbrooke’s Hospital in Cambridge used this approach to identify hidden brain lesions, allowing them to offer patients surgery that could cure their condition.

7T MRI scanners, named for their use of a 7 Tesla magnetic field, which is more than twice as strong as the 3T scanners commonly used, have previously struggled with signal blackspots in key areas of the brain. However, researchers from Cambridge and Paris have developed a technique that overcomes this issue, as detailed in a study published today (March 21) in Epilepsia.

The challenge of treating focal epilepsy.

Rabah et al. discover an astrocyte-to-neuron hydrogen peroxide signalling cascade, which is crucial for long-term memory formation in Drosophila. This signalling is found to be inhibited by amyloid-β peptide, suggesting a link to Alzheimer’s disease.

Mechanism of neuroinflammation protection by astrocytes.

How astrocytes controls neuroinflammation is not clearly understood.

The researchers demonstrate that the upregulation of basic leucine zipper ATF-like transcription factor (BATF)2 downstream of IFNg regulates the inflammatory potential of astrocytes during neuroinflammation.

In vivo evidence suggests that BATF2 limits CNS autoimmunity and the expression of IFNg-driven inflammatory mediators.

Mechanistically, BATF2 binds and prevents the overexpression of IFN regulatory factor (IRF)1 and IRF1 targets such as caspase-1. Batf2−/− mice exhibit exacerbated clinical disease severity in a murine model of central nervous system autoimmunity and express increased astrocyte-specific IRF1 and caspase-1, suggesting an amplified IFN response in vivo.

They also demonstrate that BATF2 expressed primarily in astrocytes within multiple sclerosis lesions and that this expression is colocalized with IRF1.

These data suggest that BATF2 contributes to protective mechanisms in astrocytes during chronic neuroinflammation. https://sciencemission.com/BATF2-and-neuroinflammation