Study on the sleep and gait of idiopathic normal pressure hydrocephalus

脂质运载蛋白型前列腺素D合成酶（L-PGDS）是一种脑脊液（CSF）蛋白，其浓度在特发性正常压力脑积水（iNPH）中降低。L-PGDS作为一种分子伴侣，防止β淀粉样蛋白的神经毒性聚集。本研究的目的是阐明L-PGDS下降与称为不成比例扩大蛛网膜下腔脑积水（DESH）的iNPH独特形态实体的相关性。我们评估了CSF中的L-PGDS、淀粉样蛋白β和tau蛋白、临床体征、DESH的范围和实质损害的严重程度。DESH CSF中的L-PGDS和tau水平降低。L-PGDS水平与tau水平、年龄、胼胝体角度和ARWMC评分呈正相关，与额叶评估组呈负相关。我们的数据支持L-PGDS作为iNPH中DESH特征、白色损害和额叶功能障碍的替代标志物的诊断价值，并表明L-PGDS和tau蛋白之间可能存在相互作用。

Lipocalin-type prostaglandin D synthase (L-PGDS) is a cerebrospinal fluid (CSF) protein, and its concentration is decreased in idiopathic normal pressure hydrocephalus (iNPH). L-PGDS behaves as a chaperone to prevent the neurotoxic aggregation of amyloid beta. The aim of this study was to clarify the relevance of the L-PGDS decease for a unique morphological entity of iNPH called disproportionately enlarged subarachnoid-space hydrocephalus (DESH). We evaluated L-PGDS, amyloid beta and tau in CSF, the clinical signs, the extent of DESH and the severity of parenchymal damage. L-PGDS and tau levels were decreased in DESH CSF. L-PGDS levels correlated positively with tau levels, age, callosal angle, and ARWMC scores, and negatively with frontal assessment battery. Our data support the diagnostic value of L-PGDS as a surrogate marker for DESH features, white matter damage, and frontal lobe dysfunction in iNPH, and suggest a possible interaction between L-PGDS and tau protein.