德国一家多发性硬化症研究机构KKNMS17日发表公报说，研究人员开发出治疗多发性硬化症的新方法。
公报说，研究人员首先以老鼠为实验对象，发现如果免疫系统的T细胞和巨噬细胞缺乏脑源性神经营养因子，神经细胞受侵害会加重，从而证实脑源性神经营养因子对神经细胞有保护作用。
由于人造脑源性神经营养因子很难进入脑部，研究人员于是将T细胞与人造脑源性神经营养因子“捆绑”后，将后者“护送”过脑血管障蔽，使其顺利到达脑部发挥作用。
另外，研究人员还证实现有的治疗多发性硬化症药物Glatirameracetat不仅有抑制炎症的作用，而且有助于脑源性神经营养因子的产生。多项特点使这种新疗法在多发性硬化症治疗中有很大应用潜力。
这一成果发表在最新一期英国《大脑》杂志上。
推荐原文出处：
Brain doi:10.1093/brain/awq179
Functional role of brain-derived neurotrophic factor in neuroprotective autoimmunity: therapeutic implications in a model of multiple sclerosis
Ralf A. Linker1,*, De-Hyung Lee1 ,*, Seray Demir1,2 ,*, Stefan Wiese3, Niels Kruse2, Ines Siglienti1, Ellen Gerhardt4, Harald Neumann5, Michael Sendtner6,, Fred Lühder2, and Ralf Gold1,
Brain-derived neurotrophic factor plays a key role in neuronal and axonal survival. Brain-derived neurotrophic factor is expressed in the immune cells in lesions of experimental autoimmune encephalomyelitis and multiple sclerosis, thus potentially mediating neuroprotective effects. We investigated the functional role of brain-derived neurotrophic factor in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Mice deficient for brain-derived neurotrophic factor in immune cells displayed an attenuated immune response in the acute phase of experimental autoimmune encephalomyelitis, but progressive disability with enhanced axonal loss in the chronic phase of the disease. In mice deficient for central nervous system-derived brain-derived neurotrophic factor via glial fibrillary acidic protein-crescentin-mediated deletion, a more severe course of experimental autoimmune encephalomyelitis and an overall increased axonal loss was observed. In a lentiviral approach, injection of brain-derived neurotrophic factor-overexpressing T cells led to a less severe course of experimental autoimmune encephalomyelitis and direct axonal protection. Our data imply a functional role of brain-derived neurotrophic factor in autoimmune demyelination by mediating axon protection.
