Astrocytic FABP5 drives cerebellar white matter dysfunction in multiple system atrophy by promoting TNF signaling and ferroptosis

This study identifies astrocytic FABP5 as a critical mediator linking glial inflammation, ferroptosis, and mitochondrial dysfunction in multiple system atrophy pathogenesis. Overall design: Primary mouse astrocytes were treated with LPS or subjected to shFABP5 silencing under LPS stimulation to investigate transcriptomic alterations associated with FABP5-regulated neuroinflammation and ferroptosis.