Table of Contents
Epilepsy Research and Treatment
Volume 2011 (2011), Article ID 258365, 6 pages
http://dx.doi.org/10.1155/2011/258365
Research Article

ADAM23, a Gene Related to LGI1, Is Not Linked to Autosomal Dominant Lateral Temporal Epilepsy

1CNR-Institute of Neurosciences, Section of Padua, Department of Experimental Biomedical Sciences, University of Padua, viale G. Colombo 3, 35121 Padova, Italy
2Department of Biology, University of Padua, Padova, Italy
3Department of Neurological Sciences, La Sapienza University, Roma, Italy
4Department of Neurological Sciences, Federico II University, Napoli, Italy
5Department of Neurosciences, Bellaria Hospital, Bologna, Italy
6Muscular and Neurodegenerative Disease Unit, Institute “G. Gaslini”, University of Genova, 16147 Genova, Italy
7Clinic of Neurology, University of Bari, Italy
8Department of Pediatrics, University of Padua, Padova, Italy
9Institute of Neurology, University Magna Graecia, Catanzaro, Italy
10Ospedale di Circolo, Varese, Italy
11Foundation Neurological Institute “C. Besta”, Milano, Italy
12Division of Neurology, Loreto Nuovo Hospital, Napoli, Italy

Received 16 September 2010; Accepted 1 December 2010

Academic Editor: A. Vezzani

Copyright © 2011 Laura Rigon et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Autosomal dominant lateral temporal epilepsy (ADTLE) is an inherited epileptic syndrome characterized by ictal auditory symptoms or aphasia, negative MRI findings, and relatively benign evolution. Mutations responsible for ADLTE have been found in the LGI1 gene. The functions of the Lgi1 protein apparently are mediated by interactions with members of the ADAM protein family: it binds the postsynaptic receptor ADAM22 to regulate glutamate-AMPA currents at excitatory synapses and also the ADAM23 receptor to promote neurite outgrowth in vitro and dendritic arborization in vivo. Because alteration of each of these neuronal mechanisms may underlie ADLTE, ADAM22 and ADAM23 are candidate genes for this syndrome. In a previous work, we excluded a major role of ADAM22 in the aetiology of ADLTE. Here, we performed linkage analysis between microsatellite markers within or flanking the ADAM23 gene and ADLTE in 13 Italian families. The results exclude ADAM23 as major causative gene for ADLTE.