Reelin, tau phosphorylation and psychiatric complications in patients with hippocampal sclerosis and structural abnormalities in temporal lobe epilepsy

被引:15
|
作者
Andrade Machado, Rene [1 ]
Benjumea-Cuartas, Vanesa [2 ]
Zapata Berruecos, Jose Fernando [2 ]
Matilde Agudelo-Flores, Piedad [3 ]
Maria Salazar-Pelaez, Lina [3 ]
机构
[1] Neuromedica, Antioquia, Colombia
[2] Univ CES, Escuela Grad, Grp Invest Ciencias Basicas, Neurol Inst Colombia, Antioquia, Colombia
[3] Univ CES, Escuela Grad, Grp Invest Ciencias Basicas, Antioquia, Colombia
关键词
Reelin; Temporal lobe epilepsy; Dysplasia type IIIa; Tau; Depression; Psychosis; GRANULE CELL DISPERSION; CONSENSUS CLASSIFICATION; HYPERPHOSPHORYLATED TAU; SYNTHASE KINASE-3-BETA; DENTATE GYRUS; TASK-FORCE; MIGRATION; NEURONS; PROTEIN; ROLES;
D O I
10.1016/j.yebeh.2019.04.052
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Introduction: Temporal lobe epilepsy (RE) 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 gyros, and its deficit causes dentate gyms abnormalities, which in turn has been associated with memory deficits in patients with TLE. A decreased in the expression of RELN ribonucleic add (RNA) was found in patients with TLE and dysplasia type lila 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. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码:192 / 199
页数:8
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