Neuron-specific enolase and tau protein as neurobiochemical markers of neuronal damage are related to early clinical course and long-term outcome in acute ischemic stroke

Wunderlich, Michael T.; Lins, Hartmut; Skalej, Martin; Wallesch, Claus‐W.; Goertler, Michael

doi:10.1016/j.clineuro.2005.12.006

Cited by 139 publications

(112 citation statements)

References 29 publications

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“…Missier confirmed this prediction, showing elevated levels of S-100B and NSE were associated with final infarct volume [48]. Other studies have associated infarct volume with S-100B [49,50] , NSE [50,51], Tau [51] and glutamate [52]. A larger infarct volume might also lead to a greater inflammatory response to the ischemic tissue.…”

Section: Biomarkers Of Final Infarct Volume and Outcomementioning

confidence: 75%

Blood Biomarkers of Ischemic Stroke

2011

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This review provides a summary of the protein and RNA biomarkers that have been studied for the diagnosis and assessment of ischemic stroke. Many of the biomarkers identified relate to the pathophysiology of ischemic stroke, including ischemia of CNS tissue, acute thrombosis and inflammatory response. These biomarkers are summarized by their intended clinical application in ischemic stroke including diagnosis, prediction of stroke severity and outcome, and stratification of patients for stroke therapy. Among the biomarkers discussed are recent whole genome studies using RNA expression profiles to diagnose ischemic stroke and stroke etiology. Though many candidate blood based biomarkers for ischemic stroke have been identified, none are currently used in clinical practice. With further well designed study and careful validation, the development of blood biomarkers to improve the care of patients with ischemic stroke may be achieved.

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Section: Biomarkers Of Final Infarct Volume and Outcomementioning

confidence: 75%

Blood Biomarkers of Ischemic Stroke

2011

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“…Previous studies have reported that the concentration of serum-tau was elevated in patients with acute neurologic disorders, such as stroke, and it was below the detection limit in neurologically healthy participants [18][19]. Little is known about the passage of tau from the brain into the blood.…”

Section: Discussionmentioning

confidence: 99%

Serum tau protein as a marker for the diagnosis of Creutzfeldt-Jakob disease

et al. 2011

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Total tau protein (t-tau) levels in cerebrospinal fluid (CSF) (CSF-tau) are markedly elevated in patients with Creutzfeldt-Jakob disease (CJD). Some CSF-tau may leak into the blood. We evaluated t-tau levels in serum (serum-tau) as a possible marker for the differential diagnosis of CJD from Alzheimer's disease (AD) and other rapidly progressive dementias (RPD). Serum-and CSF-tau levels were determined in patients with sporadic CJD (n = 12), AD (n = 10) and RPD but no CJD (non-CJD-RPD; n =9) who showed RPD fulfilling the WHO criteria for possible CJD at onset and had a final diagnosis other than CJD. We also analyzed serum-tau levels in healthy volunteers as a control group (n = 10). Serum-as well as CSF-tau levels were significantly elevated in CJD group compared to those in AD, non-CJD-RPD and healthy control groups. Serumtau would be a simple and useful marker to distinguish CJD from AD and non-CJD-RPD, requiring further large study to confirm this.

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“…Under normal circumstances, NSE content is not high in blood, however, along with the necrosis of neurons and the disintegration of nerve myelin, NSE is released into CSF from the cells after cerebral ischemia injury, and then leaks into blood through the blood brain barrier. The more severe the brain tissue is injured, the more nerve cells are damaged, and the more NSE is released into the blood, therefore, the detection of changes of NSE levels in CSF or in serum becomes diagnosis markers of neuronal damage [20]. Normal MBP content in CSF is less than 6.95 mg/L, however, when the ischemic cerebral injury happens, cerebral ischemia and hypoxia may be due to oligodendrocyte death and demyelination.…”

Section: Discussionmentioning

confidence: 99%

To Optimize the Therapeutic Dose and Time Window of Picroside II in Cerebral Ischemic Injury in Rats by Orthogonal Test

Huang¹,

Sun²,

Wang³

et al. 2013

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The paper aims to optimize the therapeutic dose and time window of picroside II by orthogonal test in cerebral ischemic injury in rats. The forebrain ischemia models were established by bilateral common carotid artery occlusion (BCCAO) methods. The successful models were randomly divided into sixteen groups according to orthogonal experimental design and treated by injecting picroside II intraperitonenally at different ischemic time with different dose. The concentrations of neuron-specific enolase (NSE), neuroglial marker protein S100B and myelin basic protein (MBP) in serum were determined by enzyme linked immunosorbent assay to evaluate the therapeutic effect of picroside II in cerebral ischemic injury. The results indicated that best therapeutic time window and dose of picroside II in cerebral ischemic injury were ischemia 1.5 h with 20 mg/kg body weight according to the concentrations of NSE, S100B and MBP in serum. It is concluded that according to the principle of lowest therapeutic dose with longest time window, the optimized therapeutic dose and time window are injecting picroside II intraperitonenally with 20 mg/kg body weight at ischemia 1.5 h in cerebral ischemic injury in rats.

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Neuron-specific enolase and tau protein as neurobiochemical markers of neuronal damage are related to early clinical course and long-term outcome in acute ischemic stroke

Cited by 139 publications

References 29 publications

Blood Biomarkers of Ischemic Stroke

Blood Biomarkers of Ischemic Stroke

Serum tau protein as a marker for the diagnosis of Creutzfeldt-Jakob disease

To Optimize the Therapeutic Dose and Time Window of Picroside II in Cerebral Ischemic Injury in Rats by Orthogonal Test

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