Neuron Specific Enolase, S100-beta protein and progranulin as diagnostic biomarkers of status epilepticus

Hanin, Aurélie; Denis, Jérôme Alexandre; Frazzini, Valério; Cousyn, Louis; Imbert‐Bismut, Françoise; Rucheton, Benoît; Bonnefont‐Rousselot, Dominique; Marois, Clémence; Lambrecq, Virginie; Demeret, Sophie; Navarro, Vincent

doi:10.1007/s00415-022-11004-2

Cited by 21 publications

(12 citation statements)

References 28 publications

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“…Certainly, this factor could have influenced our results and the discrepancies found with the previous studies. Associations between S100B and candidate genes for dyslexia have been reported [ 68 , 69 ]; in patients suffering from status epilepticus, significantly-increased levels of S100B were found in comparison with controls or patients with pharmacoresistant epilepsy [ 70 ]. Indeed, the administration of arundic acid (an S100B inhibitor) to murine models of epilepsy reduced neuroinflammation and improved astrocytic function after status epilepticus [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

Is S100B Involved in Attention-Deficit/Hyperactivity Disorder (ADHD)? Comparisons with Controls and Changes Following a Triple Therapy Containing Methylphenidate, Melatonin and ω-3 PUFAs

et al. 2023

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Background: Increasing evidence supports a neuroinflammatory basis in ADHD damaging glial function and thereby altering dopaminergic (DA) neurotransmission. Previous studies focusing on the S100B protein as a marker of glial function have shown contradictory results. We conducted a clinical trial to investigate differences in S100B levels between ADHD patients and controls, as well as observe gradual changes in S100B concentrations after a triple therapy (TT) containing methylphenidate (MPH), melatonin (aMT) and omega-3 fatty acids (ω-3 PUFAs). Methods: 62 medication-naïve children with ADHD (ADHD-G) and 65 healthy controls (C-G) were recruited. Serum S100B was measured at baseline (T0) in ADHD-G/C-G, and three (T3) and six months (T6) after starting TT in the ADHD-G, together with attention scores. Results: A significant increase in S100B was observed in the ADHD-G vs. C-G. In the ADHD-G, significantly higher S100B values were observed for comparisons between T0–T3 and between T0–T6, accompanied by a significant improvement in attention scores for the same timepoint comparisons. No significant differences were found for S100B between T3–T6. Conclusion: Our results agree with the hypothesis of glial damage in ADHD. Further studies on the link between DA and S100B are required to explain the transient increase in S100B following TT.

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Section: Discussionmentioning

confidence: 99%

Is S100B Involved in Attention-Deficit/Hyperactivity Disorder (ADHD)? Comparisons with Controls and Changes Following a Triple Therapy Containing Methylphenidate, Melatonin and ω-3 PUFAs

et al. 2023

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“…La neurogranina es un biomarcador prometedor pero del que por el momento no se dispone de suficiente evidencia 41 . Otros como el S100B o incluso enolasa, han mostrado cierto valor en el diagnóstico de situaciones de EE 42 .…”

Section: Diagnóstico De La Ceunclassified

Recommendations for prescribing pharmacologic prevention during emergency department treatment of epileptic seizures

Fernández Alonso,

Alonso Avilés,

González Martínez

et al. 2024

Rev Esp Urg Emerg

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“…Besides, CSF progranulin was documented to be increased in epileptic patients following status epilepticus compared to control 120 . A cohort study on patients with resistance epilepsy ( n = 56) revealed that CSF progranulin level was increased compared to healthy subjects ( n = 36) 122 . Of note, metformin activates the expression of neuroprotective and anti‐inflammatory progranulin 123 .…”

Section: The Mechanistic Role Of Metformin In Epilepsymentioning

confidence: 99%

New insights on the potential anti‐epileptic effect of metformin: Mechanistic pathway

Alnaaim,

Al‐kuraishy,

Al‐Gareeb

et al. 2023

J Cellular Molecular Medi

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Epilepsy is a chronic neurological disease characterized by recurrent seizures. Epilepsy is observed as a well‐controlled disease by anti‐epileptic agents (AEAs) in about 69%. However, 30%–40% of epileptic patients fail to respond to conventional AEAs leading to an increase in the risk of brain structural injury and mortality. Therefore, adding some FDA‐approved drugs that have an anti‐seizure activity to the anti‐epileptic regimen is logical. The anti‐diabetic agent metformin has anti‐seizure activity. Nevertheless, the underlying mechanism of the anti‐seizure activity of metformin was not entirely clarified. Henceforward, the objective of this review was to exemplify the mechanistic role of metformin in epilepsy. Metformin has anti‐seizure activity by triggering adenosine monophosphate‐activated protein kinase (AMPK) signalling and inhibiting the mechanistic target of rapamycin (mTOR) pathways which are dysregulated in epilepsy. In addition, metformin improves the expression of brain‐derived neurotrophic factor (BDNF) which has a neuroprotective effect. Hence, metformin via induction of BDNF can reduce seizure progression and severity. Consequently, increasing neuronal progranulin by metformin may explain the anti‐seizure mechanism of metformin. Also, metformin reduces α‐synuclein and increases protein phosphatase 2A (PPA2) with modulation of neuroinflammation. In conclusion, metformin might be an adjuvant with AEAs in the management of refractory epilepsy. Preclinical and clinical studies are warranted in this regard.

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Neuron Specific Enolase, S100-beta protein and progranulin as diagnostic biomarkers of status epilepticus

Cited by 21 publications

References 28 publications

Is S100B Involved in Attention-Deficit/Hyperactivity Disorder (ADHD)? Comparisons with Controls and Changes Following a Triple Therapy Containing Methylphenidate, Melatonin and ω-3 PUFAs

Is S100B Involved in Attention-Deficit/Hyperactivity Disorder (ADHD)? Comparisons with Controls and Changes Following a Triple Therapy Containing Methylphenidate, Melatonin and ω-3 PUFAs

Recommendations for prescribing pharmacologic prevention during emergency department treatment of epileptic seizures

New insights on the potential anti‐epileptic effect of metformin: Mechanistic pathway

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