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脑源性神经营养因子(BDNF)的Val66Met多态性与多发性硬化症无关联。

No association of the Val66Met polymorphism of brain-derived neurotrophic factor (BDNF) to multiple sclerosis.

作者信息

Blanco Y, Gómez-Choco M, Arostegui J L, Casanova B, Martínez-Rodríguez J E, Boscá I, Munteis E, Yagüe J, Graus F, Saiz A

机构信息

Service of Neurology, Hospital Clinic, Universitat de Barcelona, Villarroel 170, 08036 Barcelona, Spain.

出版信息

Neurosci Lett. 2006 Apr 3;396(3):217-9. doi: 10.1016/j.neulet.2005.11.032. Epub 2005 Dec 13.

Abstract

Brain-derived neurotrophic factor (BDNF), a neurotrophin produced by neurons and immune cells, promotes neuronal survival and repair during development and after CNS injury. The BDNF-Val66Met polymorphism is functional and induces abnormal intracellular trafficking and decreased BDNF release. Therefore, we investigated the impact of the BDNF-Val66Met polymorphism on the susceptibility and clinical course in a case-control study of 224 multiple sclerosis (MS) Spanish patients and 177 healthy controls. We found no evidence for association to susceptibility or severity of the disease in our population. Moreover, we did not observe, in a subgroup of 12 MS patients, that the methionine substitution at position 66 in the prodomain had negative impact in the capacity to produce BDNF by peripheral blood mononuclear cells (PBMC).

摘要

脑源性神经营养因子(BDNF)是一种由神经元和免疫细胞产生的神经营养因子,在发育过程中和中枢神经系统损伤后促进神经元的存活和修复。BDNF-Val66Met多态性具有功能性,可导致细胞内运输异常并减少BDNF释放。因此,我们在一项对224例西班牙多发性硬化症(MS)患者和177名健康对照的病例对照研究中,调查了BDNF-Val66Met多态性对易感性和临床病程的影响。我们没有发现该多态性与我们研究人群中疾病的易感性或严重程度相关的证据。此外,在12例MS患者的亚组中,我们也未观察到前结构域第66位的甲硫氨酸替代对外周血单核细胞(PBMC)产生BDNF的能力有负面影响。

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