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Reduction of hippocampal collapsin response mediated protein-2 in patients with mesial temporal lobe epilepsy
Thomas Czech1, Jae-Won Yang, Edina Csaszar
1Department of Neurosurgery, University of Vienna, Waehringer Guertel 18, A-1090 Vienna, Austria.
Abstract:
Although the syndrome of mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis has been elaborated in recent years, pathogenesis and pathomechanisms are still elusive. Performing protein hunting in hippocampus of patients with MTLE we detected derangement of collapsin response mediated protein-2 (CRMP-2). Hippocampal tissue from controls and MTLEs was taken and two-dimensional gel electrophoresis with subsequent MALDI-MS-characterisation was applied. The proteomic approach identified 13 spots unambiguously assigned to CRMP-2. Three spots at molecular weight 55 kDa showed a significant decrease in MTLE and other 3 spots at 65 kDa showed deranged in MTLE. Immunoblotting revealed two bands at 65 and 55 kDa in the control group whereas the 55 kDa band was extremely low expressed in MTLE. CRMP-2 is required to induce axonal outgrowth and maintaining neuronal polarity in hippocampal neurons and the significant decrease of this protein may represent or underlie impaired neuronal plasticity, neurodegeneration, wiring of the brain in MTLE and may explain abnormal migration. Therefore, the decrease of CRMP-2 may well contribute to the understanding of the still unclear pathomechanisms involved in MTLE.
Insights
Mesial temporal lobe epilepsy (MTLE) involves altered collapsin response mediated protein-2 (CRMP-2) in the hippocampus. Reduced CRMP-2 may underlie neurodegeneration and impaired brain wiring in MTLE patients.
Area of Science:
- Neuroscience
- Proteomics
- Epilepsy Research
Background:
- Mesial temporal lobe epilepsy (MTLE) pathogenesis remains unclear despite recent advances.
- Hippocampal sclerosis is a common hallmark of MTLE, suggesting crucial roles for hippocampal dysfunction.
Purpose of the Study:
- To investigate protein alterations in the hippocampus of MTLE patients.
- To identify specific proteins involved in MTLE pathomechanisms.
Main Methods:
- Proteomic analysis using two-dimensional gel electrophoresis and MALDI-MS on hippocampal tissue from MTLE patients and controls.
- Immunoblotting to confirm protein expression levels.
Main Results:
- Derangement of collapsin response mediated protein-2 (CRMP-2) was detected in MTLE hippocampi.
- A significant decrease in 55 kDa CRMP-2 spots and altered 65 kDa CRMP-2 spots were observed in MTLE.
- Immunoblotting confirmed extremely low expression of the 55 kDa CRMP-2 band in MTLE.
Conclusions:
- Reduced CRMP-2 levels in MTLE may indicate impaired neuronal plasticity, neurodegeneration, and abnormal brain wiring.
- CRMP-2 deficiency could contribute to the pathomechanisms underlying MTLE and abnormal neuronal migration.
