Reelin, tau phosphorylation and psychiatric complications in patients with hippocampal sclerosis and structural abnormalities in temporal lobe epilepsy
| Autor: | Vanesa Benjumea-Cuartas, José Fernando Zapata Berruecos, Piedad Matilde Agudelo-Flóres, Lina María Salazar-Peláez, René Andrade Machado |
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| Rok vydání: | 2019 |
| Předmět: |
Pathology
medicine.medical_specialty Cell Adhesion Molecules Neuronal Nerve Tissue Proteins tau Proteins Hippocampus Temporal lobe 03 medical and health sciences Behavioral Neuroscience Epilepsy 0302 clinical medicine medicine Humans 030212 general & internal medicine Reelin Phosphorylation Neurons Extracellular Matrix Proteins Memory Disorders Hippocampal sclerosis Sclerosis biology business.industry Dentate gyrus Serine Endopeptidases Brain Human brain Cortical dysplasia medicine.disease Reelin Protein medicine.anatomical_structure Epilepsy Temporal Lobe nervous system Neurology Dysplasia biology.protein Neurology (clinical) business 030217 neurology & neurosurgery |
| Zdroj: | Epilepsy & Behavior. 96:192-199 |
| ISSN: | 1525-5050 |
| Popis: | Introduction Temporal lobe epilepsy (TLE) is the most common adult epileptic syndrome. About 30–70% of those cases have neuropsychiatric complications. More than 10% of patients have TLE because of focal cortical dysplasia (FCD) type IIIa. Objectives The objective of this study was to review the evidence of reelin (RELN) deficiency and tau phosphorylation role in the histopathological, neuropsychiatric, and hyperexcitability features in TLE because of dysplasia type IIIa. Methods The current literature was reviewed using Cochrane, EMBASE, PROSPERO, MEDLINE, and PubMed from 1995 to July 2018. Articles of interest were reviewed by one investigator (RAM). Results Reelin deficit is related to an abnormal migration of neurons in dentate gyrus, and its deficit causes dentate gyrus abnormalities, which in turn has been associated with memory deficits in patients with TLE. A decreased in the expression of RELN ribonucleic acid (RNA) was found in patients with TLE and dysplasia type IIIa compared with patients with TLE and isolated hippocampal sclerosis (HS). Reelin might affect the distribution and dynamic instability of microtubules within neurons in the cerebral cortex and their phosphorylation. Amyloid pathology, tauopathy, or phosphorylated tau (p-tau) overexpression has been reported in epileptic human brain and in animal models of epilepsy. Conclusion Reelin deficit may determine an abnormal cortical lamination and dentate gyrus dispersion and might be associated with an abnormal tau phosphorylation. These processes can be associated with an abnormal hyperexcitability, neuropsychiatric complications, and a myriad of typical histopathological features seen in patients with TLE because of dysplasia type IIIa. |
| Databáze: | OpenAIRE |
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