Topic: PLP1Tg

Lipid-rich myelin membranes are a major target of immune attacks in chronic neurological disorders such as multiple sclerosis (MS). Following an acute demyelinating event, damaged myelin is cleared by phagocytes and new myelin sheaths are generated from existing or newly differentiated oligodendrocytes. Our previous studies shed light on the critical impact of functional lipid recycling pathways within phagocytes to enable remyelination of acute lesion. However, to date it is unclear how chronic progressive disease is linked to lipid metabolic pathways. According to the ‘inside-out’ concept of