德國一家多發(fā)性硬化癥研究機(jī)構(gòu)KKNMS17日發(fā)表公報(bào)說,，研究人員開發(fā)出治療多發(fā)性硬化癥的新方法。
公報(bào)說,，研究人員首先以老鼠為實(shí)驗(yàn)對象,，發(fā)現(xiàn)如果免疫系統(tǒng)的T細(xì)胞和巨噬細(xì)胞缺乏腦源性神經(jīng)營養(yǎng)因子，神經(jīng)細(xì)胞受侵害會(huì)加重,，從而證實(shí)腦源性神經(jīng)營養(yǎng)因子對神經(jīng)細(xì)胞有保護(hù)作用,。
由于人造腦源性神經(jīng)營養(yǎng)因子很難進(jìn)入腦部，研究人員于是將T細(xì)胞與人造腦源性神經(jīng)營養(yǎng)因子“捆綁”后,，將后者“護(hù)送”過腦血管障蔽,，使其順利到達(dá)腦部發(fā)揮作用。
另外,，研究人員還證實(shí)現(xiàn)有的治療多發(fā)性硬化癥藥物Glatirameracetat不僅有抑制炎癥的作用,，而且有助于腦源性神經(jīng)營養(yǎng)因子的產(chǎn)生。多項(xiàng)特點(diǎn)使這種新療法在多發(fā)性硬化癥治療中有很大應(yīng)用潛力,。
這一成果發(fā)表在最新一期英國《大腦》雜志上,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
