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      Ubiquitin Carboxy-Terminal Hydrolase L1 (UCH-L1) is increased in cerebrospinal fluid and plasma of patients after epileptic seizure

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          Abstract

          Background

          Clinical and experimental studies have demonstrated that seizures can cause molecular and cellular responses resulting in neuronal damage. At present, there are no valid tests for assessing organic damage to the brain associated with seizure. The aim of this study was to investigate cerebrospinal fluid (CSF) and plasma concentrations of Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), a sensitive indicator of acute injury to brain neurons, in patients with tonic–clonic or partial secondarily generalized seizures due to various etiologies.

          Methods

          CSF and plasma concentrations of UCH-L1 were assessed in 52 patients within 48 hours after epileptic seizure and in 19 controls using ELISA assays.

          Results

          CSF obtained within 48 hours after seizure or status epilepticus (SE) presented significantly higher levels of UCH-L1 compared to controls (p = 0.008). Plasma UCH-L1 concentrations were negatively correlated with time to sample withdrawal. An analysis conducted using only the first 12 hours post-seizure revealed significant differences between concentrations of UCH-L1 in plasma and controls (p = 0.025). CSF and plasma concentrations were strongly correlated with age in patients with seizure, but not in control patients. Plasma UCH-L1 levels were also significantly higher in patients after recurrent seizures (n = 4) than in those after one or two seizures (p = 0.013 and p = 0.024, respectively).

          Conclusion

          Our results suggest that determining levels of neuronal proteins may provide valuable information on the assessment of brain damage following seizure. These data might allow clinicians to make more accurate therapeutic decisions, to identify patients at risk of progression and, ultimately, to provide new opportunities for monitoring therapy and targeted therapeutic interventions.

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          Most cited references30

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          Is epilepsy a progressive disorder? Prospects for new therapeutic approaches in temporal-lobe epilepsy.

          During the past decade, it has become apparent that neural circuits undergo activity-dependent reorganisation. In pathological disorders with recurring episodes of excessive neural activity, such as temporal-lobe epilepsy, brain circuits can undergo continual remodelling. For clinical practice, seizure-induced remodelling implies that after a diagnosis of epilepsy, recurring seizures can cause continuing neural reorganisation and potentially contribute to progressive severity of the epilepsy and to cognitive and behavioural consequences. The alterations induced by seizures include neuronal death and birth, axonal and dendritic sprouting, gliosis, molecular reorganisation of membrane and extracellular-matrix proteins, and intermediates involved in cellular homoeostasis. These changes are influenced by genetic background and seizure type, thus identification of genetic risk factors should be a priority. Therapeutic modification of seizure-induced molecular and cellular responses offers new opportunities for intervention beyond seizure suppression.
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            Molecular and cellular basis of epileptogenesis in symptomatic epilepsy.

            Epileptogenesis refers to a process in which an initial brain-damaging insult triggers a cascade of molecular and cellular changes that eventually lead to the occurrence of spontaneous seizures. Cellular alterations include neurodegeneration, neurogenesis, axonal sprouting, axonal injury, dendritic remodeling, gliosis, invasion of inflammatory cells, angiogenesis, alterations in extracellular matrix, and acquired channelopathies. Large-scale molecular profiling of epileptogenic tissue has provided information about the molecular pathways that can initiate and maintain cellular alterations. Currently we are learning how these pathways contribute to postinjury epileptogenesis and recovery process and whether they could be used as treatment targets.
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              • Article: not found

              PGP 9.5--a new marker for vertebrate neurons and neuroendocrine cells.

              PGP 9.5 is a new cytoplasmic neuron-specific protein structurally and immunologically distinct from neuron-specific enolase. A specific antiserum has now shown that this protein is widely distributed in vertebrate brains and is also present in cells of the human diffuse neuroendocrine system. PGP 9.5 appears to be older than neuron-specific enolase in evolutionary terms, as an immunologically-related protein can be found in species as remote as the trout.
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                Author and article information

                Journal
                BMC Neurol
                BMC Neurol
                BMC Neurology
                BioMed Central
                1471-2377
                2012
                29 August 2012
                : 12
                : 85
                Affiliations
                [1 ]Banyan Biomarkers, Inc., 113400 Progress Blvd, Alachua, FL, 32615, USA
                [2 ]Department of Neurology, Tampere University Hospital, P.O.Box 2000, Tampere, FIN-33521, Finland
                [3 ]Clinical Department, Banyan Biomarkers Inc., 12085 Research Dr, Alachua, FL, 32615, USA
                Article
                1471-2377-12-85
                10.1186/1471-2377-12-85
                3500207
                22931063
                9cb41a9a-50fd-4a17-b63b-ea473957f161
                Copyright ©2012 Mondello et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 8 February 2012
                : 24 August 2012
                Categories
                Research Article

                Neurology
                uch-l1,epileptic seizures,biomarkers,neuronal damage
                Neurology
                uch-l1, epileptic seizures, biomarkers, neuronal damage

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