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

It could help patients regain movement by targeting brain rhythms.

Scientists found that aggressive lung cancer cells create their own electrical network, helping them spread. This unique trait may reveal new treatment opportunities. Researchers at the Francis Crick Institute have discovered that certain aggressive lung cancer cells can form their own electrical

A study from Emory University suggests that levodopa, a medication that increases dopamine levels in the brain, may help treat individuals with depression who experience motivational impairments due to high inflammation. Researchers found that a common blood test measuring C-reactive protein (CRP), a blood biomarker of inflammation produced by the liver, could help determine which patients are most likely to respond to repeated doses of levodopa.

The findings, published in the March 2025 print edition of Brain, Behavior and Immunity, show that in participants with CRP levels above 2 mg/L, daily administration of levodopa improved connectivity within a key brain reward pathway—the ventral striatum to the ventromedial prefrontal cortex —after just one week of treatment across a range of doses.

While about half of the participants responded best to a lower dose of 150 mg/day, the other half required up to 450 mg/day for levodopa to effectively overcome the effects of inflammation on this dopamine-rich reward circuit.