Time-Dependent Decrease of Clusterin as a Potential Cerebrospinal Fluid Biomarker for Drug-Resistant Epilepsy

Yu, Wei; Chen, Dan; Wang, Zhihua; Zhou, Chunlei; Luo, Jie; Xu, Yali; Shen, Lan; Yin, Huan; Tao, Shuxin; Xiao, Zheng; Xiao, Fei; Lü, Yang; Wang, Xuefeng

doi:10.1007/s12031-014-0237-3

Cited by 16 publications

(6 citation statements)

References 27 publications

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“…Additionally, according to Yu et al. (30), the CLU concentration was decreased in the CSF of human models diagnosed with epilepsy. Therefore, measurement of CLU concentrations in the CSF may be helpful in generating differential diagnosis of neurodegenerative disorders (31).…”

Section: Discussionmentioning

confidence: 92%

Clusterin as a potential marker of brain ischemia-reperfusion injury in patients undergoing carotid endarterectomy

Iłżecka

Iłżecki

Grabarska

et al. 2019

Upsala Journal of Medical Sciences

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Introduction: Carotid endarterectomy (CEA) is a surgical procedure used in the prevention of ischemic stroke. However, this procedure can cause complications of ischemia-reperfusion injury to the brain. Clusterin (CLU) is a cytoprotective chaperone protein that is released from neurons in response to various neurological injuries. The objective of the study was to report the changes in serum CLU concentrations of patients undergoing CEA.Materials and methods: The study involved 25 patients with severe internal carotid artery stenosis. Serum samples were taken from patients at three different times: within 24 hours preoperatively to CEA, 12 hours postoperatively, and 48 hours postoperatively. Serum CLU concentrations were measured using a commercially available enzyme-linked immunosorbent assay.Results: When compared to concentrations preoperatively, the serum CLU concentration initially decreased during the 12 hours following CEA. However, 48 hours following the procedure there was an increase in the CLU concentration. After statistical analysis, differences were detected in serum CLU concentration between all three recorded measurements (P < 0.05).Conclusion: Data from our study indicate that serum CLU concentrations are affected after CEA. We hypothesize that serum CLU concentrations may depend on brain ischemia-reperfusion injury following this surgical procedure.

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Section: Discussionmentioning

confidence: 92%

Clusterin as a potential marker of brain ischemia-reperfusion injury in patients undergoing carotid endarterectomy

Iłżecka

Iłżecki

Grabarska

et al. 2019

Upsala Journal of Medical Sciences

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“…For instance, previous studies of patients with epilepsy demonstrated increased clusterin mRNA expression levels in the temporal lobe tissue 47 . Still, several epilepsy studies have shown a 20–30% reduction in serum clusterin levels in patient with “idiopathic temporal lobe epilepsy” or “idiopathic epilepsy” 27,28 . So far, none of the previous studies has analysed clusterin as a biomarker for post-traumatic epilepsy.…”

Section: Discussionmentioning

confidence: 99%

Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

Gupta

Lipponen

Paldanius

et al. 2019

Sci Rep

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Progress in the preclinical and clinical development of neuroprotective and antiepileptogenic treatments for traumatic brain injury (TBI) necessitates the discovery of prognostic biomarkers for post-injury outcome. Our previous mRNA-seq data revealed a 1.8–2.5 fold increase in clusterin mRNA expression in lesioned brain areas in rats with lateral fluid-percussion injury (FPI)-induced TBI. On this basis, we hypothesized that TBI leads to increases in the brain levels of clusterin protein, and consequently, increased plasma clusterin levels. For evaluation, we induced TBI in adult male Sprague-Dawley rats (n = 80) by lateral FPI. We validated our mRNA-seq findings with RT-qPCR, confirming increased clusterin mRNA levels in the perilesional cortex (FC 3.3, p < 0.01) and ipsilateral thalamus (FC 2.4, p < 0.05) at 3 months post-TBI. Immunohistochemistry revealed a marked increase in extracellular clusterin protein expression in the perilesional cortex and ipsilateral hippocampus (7d to 1 month post-TBI), and ipsilateral thalamus (14d to 12 months post-TBI). In the thalamus, punctate immunoreactivity was most intense around activated microglia and mitochondria. Enzyme-linked immunoassays indicated that an acute 15% reduction, rather than an increase in plasma clusterin levels differentiated animals with TBI from sham-operated controls (AUC 0.851, p < 0.05). Our findings suggest that plasma clusterin is a candidate biomarker for acute TBI diagnosis.

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“…87-92 Neuronal and oligodendrocyte apoptosis occur in human cervical spondylotic myelopathy 93 and canine CSM 94 , and are implicated in disease progression. 3 The lower CSF clusterin concentrations identified in CSM-affected dogs may compromise neuronal and oligodendrocyte survival by promoting apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Cerebrospinal Fluid in Canine Cervical Spondylomyelopathy

Martín-Vaquero

Costa

Allen

et al. 2015

Spine

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Study Design Prospective study. Objective To identify proteins with differential expression in the cerebrospinal fluid (CSF) from 15 clinically normal (control) dogs and 15 dogs with cervical spondylomyelopathy (CSM). Summary of Background Data Canine CSM is a spontaneous, chronic, compressive cervical myelopathy similar to human cervical spondylotic myelopathy. There is a limited knowledge of the molecular mechanisms underlying these conditions. Differentially expressed CSF proteins may contribute with novel information about the disease pathogenesis in both dogs and humans. Methods Protein separation was performed with two-dimensional electrophoresis. A Student’s t-test was used to detect significant differences between groups (P < 0.05). Three comparisons were made: 1) control versus CSM-affected dogs, 2) control versus non-corticosteroid treated CSM-affected dogs, and 3) non-corticosteroid treated CSM-affected versus corticosteroid treated CSM-affected dogs. Protein spots exhibiting at least a statistically significant 1.25-fold change between groups were selected for subsequent identification with capillary-liquid chromatography tandem mass spectrometry. Results A total of 96 spots had a significant average change of at least 1.25-fold in one of the three comparisons. Compared to the CSF of control dogs, CSM-affected dogs demonstrated increased CSF expression of eight proteins including vitamin D-binding protein, gelsolin, creatine kinase B-type, angiotensinogen, alpha-2-HS-glycoprotein, SPARC, calsyntenin-1, and complement C3, and decreased expression of pigment epithelium-derived factor, prostaglandin-H2 D-isomerase, apolipoprotein E, and clusterin. In the CSF of CSM-affected dogs, corticosteroid treatment increased the expression of haptoglobin, transthyretin isoform 2, cystatin C-like, apolipoprotein E, and clusterin, and decreased the expression of angiotensinogen, alpha-2-HS-glycoprotein, and gelsolin. Conclusions Many of the differentially expressed proteins are associated with damaged neural tissue, bone turnover, and/or compromised blood-spinal cord barrier. The knowledge of the protein changes that occur in CSM and upon corticosteroid treatment of CSM-affected patients will aid in further understanding the pathomechanisms underlying this disease.

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Time-Dependent Decrease of Clusterin as a Potential Cerebrospinal Fluid Biomarker for Drug-Resistant Epilepsy

Cited by 16 publications

References 27 publications

Clusterin as a potential marker of brain ischemia-reperfusion injury in patients undergoing carotid endarterectomy

Clusterin as a potential marker of brain ischemia-reperfusion injury in patients undergoing carotid endarterectomy

Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

Proteomic Analysis of Cerebrospinal Fluid in Canine Cervical Spondylomyelopathy

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