Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal Hospital, 43180, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Neuromolecular Med. 2017 Mar;19(1):154-160. doi: 10.1007/s12017-016-8439-1. Epub 2016 Sep 19.
Stanniocalcin-1 (STC-1) is a nerve cell-enriched protein involved in intracellular calcium homeostasis regulation. Changes in calcium regulation are hypothesized to play a role in the pathophysiology of Alzheimer's disease (AD). The expression of STC-1 increases in response to ischemic stroke, but whether it is altered in neurodegenerative disorder, particularly Alzheimer's disease (AD), has not been investigated before. We measured STC-1 in cerebrospinal fluid (CSF) samples from a total of 163 individuals including AD, prodromal AD (pAD), mixed AD, stable mild cognitive impairment (sMCI), and diagnoses of other dementia than AD, as well as cognitively normal controls (CNC) enrolled at academic centers in France and Sweden. STC-1 concentration was reliably measureable in all CSF samples and was significantly increased in the initial exploratory cohort of neurochemically enriched AD patients versus AD biomarker-negative controls. In the second cohort, STC-1 was increased in AD versus pAD, and other dementia disorders, but the difference was not statistically significant. In the third cohort, there was no significant difference in STC-1 concentration between AD and CNC; however, STC-1 concentration was significantly decreased in patients with other dementia disorders compared with AD and CNC. Taken together, CSF STC-1 showed an increasing trend in AD, but the findings were not consistent across the three study cohorts. In contrast, CSF STC-1 concentrations were reduced in patients with dementia diagnoses other than AD, as compared with both AD patients and CNC. The findings from these studies suggest CSF STC-1 as a potential biomarker in differential diagnosis of dementias.
脑啡肽酶 1（STC-1）是一种富含神经细胞的蛋白质，参与细胞内钙稳态调节。钙调节的变化被认为在阿尔茨海默病（AD）的病理生理学中起作用。STC-1 的表达在缺血性中风后增加，但在神经退行性疾病，特别是阿尔茨海默病（AD）中是否发生改变尚未得到研究。我们测量了来自总共 163 名个体的脑脊液（CSF）样本中的 STC-1，这些个体包括 AD、前驱 AD（pAD）、混合 AD、稳定轻度认知障碍（sMCI）以及其他非 AD 痴呆的诊断，以及在法国和瑞典的学术中心招募的认知正常对照（CNC）。STC-1 浓度在所有 CSF 样本中均可可靠测量，并在神经化学富集的 AD 患者与 AD 生物标志物阴性对照的初始探索性队列中显著增加。在第二个队列中，AD 与 pAD 和其他痴呆症相比，STC-1 增加，但差异无统计学意义。在第三个队列中，AD 与 CNC 之间的 STC-1 浓度没有显著差异；然而，与 AD 和 CNC 相比，其他痴呆症患者的 STC-1 浓度显著降低。总之，CSF STC-1 在 AD 中呈上升趋势，但这些发现在三个研究队列中并不一致。相比之下，与 AD 患者和 CNC 相比，患有除 AD 以外的痴呆症的患者 CSF STC-1 浓度降低。这些研究的结果表明 CSF STC-1 可能是鉴别诊断痴呆症的潜在生物标志物。
