Oligodendrocyte dysfunction and regeneration failure: A novel hypothesis of delayed encephalopathy after carbon monoxide poisoning.

摘要: Abstract Carbon monoxide (CO) poisoning usually causes brain lesions and delayed encephalopathy, also known as neurological sequelae (DNS). Demyelination of white matter (WM) is one the most common sites abnormalities in patients with DNS, but its mechanisms remain unclear. Oligodendrocytes (OLs) are myelinated cells that ensure rapid conduction neuronal axon signals provide nutritional factors necessary for maintaining nerve integrity central nervous system (CNS). OLs readily regenerate replace damaged myelin membranes around axons adult mammalian CNS following demyelination. The ability to depends on availability precursor (OPCs) adults. Multiple injury-related can induce OPC expansion followed by OL differentiation, axonal contact regeneration (remyelination). Therefore, dysfunction failure deep WM key pathophysiological leading injury after CO poisoning. CO-induced toxicity may interfere function render OPCs unable through some unclear mechanisms, progressive demyelinating damage resulting DNS. In future, combination therapies reduce promote differentiation remyelination be important prevention treatment of DNS