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

• Published in: Epilepsy & behavior Vol. 96; pp. 192 - 199
• Main Authors: Machado, René Andrade, Benjumea-Cuartas, Vanesa, Zapata Berruecos, José Fernando, Agudelo-Flóres, Piedad Matilde, Salazar-Peláez, Lina María
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2019
• Subjects: Depression; Dysplasia type IIIa; Psychosis; Reelin; Tau; Temporal lobe epilepsy; SFK/Fyn/CrK; MTLE; TUBD1; Tau; p-tau; HS; VLDLR; TLE; Psychosis; Crk/C3G/Rap1; RELN; MAP2; TLS; MFS; GSK; SOCS family; CSNK2A1; BAD; Dysplasia type IIIa; FCD; PKB; Src/Fyn; GCD; Depression; LAMB1; TUBG1; ApoER2; EKR; EAK; CR; GCL; MYO1E; MEK; Reelin; P38; CDK5; RAF; MAP1A; Temporal lobe epilepsy
• ISSN: 1525-5050; 1525-5069
• DOI: 10.1016/j.yebeh.2019.04.052

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. 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. 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). 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. 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. •Reelin (RELN) deficit is associated with psychiatric and memory symptoms in patients with temporal lobe epilepsy.•A unique pattern of tau phosphorylated distribution has been found in patients with TLE.•Abnormal tau phosphorylation has been associated with different neuropsychiatric complications in patients with TLE.•The level of tau phosphorylation is increased in reelin deficient mice.