Neurology：特发性正常颅压性脑积水脑室旁代谢降低并轴索变性

特发性正常颅压性脑积水以智能障碍、运动迟缓步态、尿失禁等三主征为主要临床表现，病因尚不明确。来自瑞典的Anna Jeppsson等医生研究了特发性正常颅压脑积水患者的脑脊液生化指标，该观察性研究旨在探究特发性正常颅压脑积水(iNPH)的病理生理过程及评价脑脊液（CSF）生物标记物的诊断及对预后的评价作用。研究结果显示：特发性正常颅压脑积水患者的病理生理机制与脑室旁代谢降低及轴索变性相关，而不是主要损伤皮质。
该研究利用ELISA分析正常颅压脑积水患者及健康老年人群的腰穿脑脊液标本及iNPH患者术前及术后的脑室内脑脊液标本。分析的指标有神经丝轻链蛋白(NFL)，髓鞘碱性蛋白(MBP)，β淀粉样蛋白的异构体(Aβ38, Aβ40和 Aβ42)，可溶性淀粉样蛋白前体(sAPP)的异构体sAPPα和sAPPβ，总tau蛋白和磷酸化的tau蛋白(t-和p-tau)，炎性标记物白细胞介素8和白介素10，及单核细胞趋化因子1.
iNPH患者与正常对照组患者相比，神经丝蛋白轻链(NFL)和淀粉样蛋白前体 (APP)衍生蛋白及tau蛋白明显降低。iNPH患者术前与术后相比NFL、APP衍生蛋白、p-tau及脑室内白蛋白升高，而 MBP和t-tau蛋白含量降低。症状好转的iNPH患者与没有明显好转的患者相比，在脑室腹腔引流后APP衍生蛋白含量升高。
本研究的数据显示特发性正常颅压脑积水患者的病理生理机制与脑室旁代谢降低及轴索变性相关，而不是主要损伤皮质。

与脑脊液相关的拓展阅读：

• Neural Regen Res. ：四种细胞与脑脊液联合培养液中神经营养因子的表达
• 嗜睡者脑脊液发现“安眠”物质
• 颈前路后纵韧带骨化切除术脑脊液漏发生率高
• Arch Neurol ：5种脑脊液标志物鉴别不同类型的痴呆 更多信息请点击：有关脑脊液更多资讯

Idiopathic normal-pressure hydrocephalus: Pathophysiology and diagnosis by CSF biomarkers.
OBJECTIVES
This observational study aimed to explore the pathophysiology of idiopathic normal-pressure hydrocephalus (iNPH) and to evaluate the diagnostic and prognostic value of CSF biomarkers.
METHODS
Lumbar CSF of patients with iNPH and healthy elderly individuals (HI) and ventricular CSF (VCSF) from the patients with iNPH pre and 6 months postsurgery were analyzed by ELISA. We analyzed neurofilament light protein (NFL), myelin basic protein (MBP), a panel of β-amyloid isoforms (Aβ38, Aβ40, and Aβ42), soluble amyloid precursor protein (sAPP) isoforms sAPPα and sAPPβ, total and phosphorylated tau protein (t- and p-tau), and inflammatory markers interleukin 8, interleukin 10, and monocyte chemoattractant protein 1.
RESULTS
NFL was elevated and amyloid precursor protein (APP)-derived proteins and tau proteins were lower in patients with iNPH than in HI. Postsurgery, there was an increase of NFL, APP-derived proteins, p-tau, and albumin in VCSF, whereas levels of MBP and t-tau had decreased. Improved patients showed a greater increase of APP-derived proteins in VCSF following shunting than did those who did not improve.
CONCLUSIONS
We interpret our data as iNPH pathophysiology to be characterized by a reduced periventricular metabolism and axonal degeneration but no major cortical damage.