Rbap48 Could Act as a Candidate Biological Predictor for the Cognition Impairments of Patients with Temporal Lobe Epilepsy: A Hypothesis Based on Recent Molecular Findings

Abstract

The temporal lobe epilepsy (TLE) is characterized by the neurodegeneration, abnormal reorganization of circuitry, and the loss of functional inhibition in hippocampus regions. Particularly, the declined neurogenesis in hippocampus has emerged as a significant hallmark of TLE. RbAp48, which is initially recognized as a retinoblastoma binding protein, is also identified as a positive regulator of human neurogenesis owing to its ability to regulate the expression of the pluripotency, differentiation, and cell cycle genes in human PSCs. The deficiency of RbAp48 critically contributes to the dentate gyrus (DG) dysfunction and is closely related to age-related memory deficits. Nevertheless, the roles of RbAp48 in the neurogenesis deterioration and memory loss of TLE patients remain to be determined. In view of the linkage between the deficiency of RbAp48 and the TLE-related memory loss, it is reasonable to hypothesize that the expression level of RbAp48 in the hippocampus of the TLE patients might be down regulated in accordance with the reduced neurogenesis. As the neurogenesis exhibits a close relationship with the hippocampal functions like learning and memory, the RbAp48 would possibly act as a candidate biology predictor for the cognition impairments of the TLE patients. This notion might cast insights into the etiology of hippocampusbased memory loss in TLE patients with the potentials of opening up new therapeutic avenues.