Dong and colleagues studied the mechanisms that mediate neurodegeneration in multiple sclerosis and determined the direct role of oxidized phosphatidylcholines (OxPCs) in driving the death of central nerve cells.
The activity of microglia mediated by lipid sensor TREM2 and neutralizing OxPC antibody can rescue the neurotoxicity induced by OxPC.
Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination and neurodegenerative processes, including axonal damage, and in the most severe cases, the loss of neurons in the central nervous system.
This debilitating disease is the main cause of neurological dysfunction in young people, and most cases are diagnosed between the ages of 20-50.
No genes responsible for multiple sclerosis have been discovered; however, genome-wide association studies have identified more than 200 variants and cells involved in the adaptive and innate immune system.
The pathological feature of MS is demyelination of the brain or spinal cord, which is invaded by self-reactive adaptive immune cells.
The broad view regarding the progression of multiple sclerosis is that autoimmune lymphocytes attack and destroy myelin, making oligodendrocytes and axons easy to die, leading to subsequent neurodegeneration, but whether myelin fragments cause neurotoxicity, if Yes, the mechanism involved is unclear.
Dong et al.
pointed out in the journal Nature Neuroscience that oxidized phosphatidylcholines (OxPCs) are only present in multiple sclerosis lesions and not in the adjacent normal white matter.
Prior to this, OxPCs had been reported in MS lesions, but Dong.
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