Glutamate receptor antibodies directed against AMPA receptors subunit 3 peptide B (GluR3B) associate with some cognitive/psychiatric/behavioral abnormalities in epilepsy patients.
Antibodies (Ab's) to glutamate receptors, directed specifically against AMPA receptors subunit 3 peptide B (i.e. GluR3 amino acids 372-395), named GluR3B Ab's, can by themselves activate GluR3-containing glutamate/AMPA receptors, evoke ion currents via the receptor's ion channel, kill neurons and damage the brain. Herein we first tested 14 consecutive epilepsy patients and 10 healthy controls, and found that 7 (50%) patients had GluR3B Ab's. Second, in 71 other consecutive epilepsy patients (20 generalized epilepsy, 51 partial epilepsy) and 49 controls, we found that 17 (24%) patients had GluR3B Ab's, of which 8 had generalized and 9 partial epilepsy. We then studied 41 epilepsy patients: 21 patients with GluR3B Ab's and 20 without such Ab's (pooled of both tests without biased selection), for possible association of GluR3B Ab's with disease severity and/or neurobehavioral/cognitive comorbidities. Of the 21 patients with GluR3B Ab's, 6 had symptomatic, 7 cryptogenic, and 8 idiopathic epilepsy. Of the 20 patients without GluR3B Ab's, 16 had idiopathic etiology, and 4 nonidiopathic epilepsy. We found that among the 21 patients with GluR3B Ab's, 19 patients (90%) had learning problems, 16 (76%) attention problems, and 15 (71%) psychiatric problems. In contrast, among the 20 patients without GluR3B Ab's, only 6 (30%) had learning problems (p<0.0001), 5 (25%) attention problems (p=0.0017), and 2 (10%) psychiatric problems (p<0.0001). These findings suggest either that neurobehavioral abnormalities occur more frequently in epilepsy patients already having GluR3B Ab's, and may be due to them, or that GluR3B Ab's are more frequent in patients already having neurobehavioral abnormalities.
Epilepsy Service, Schneider Children's Medical Center of Israel, Petach Tikva, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: hagoldberg@clalit.org.il.
Hadassa
H
Goldberg-Stern
Department of Infection, Immunity and Inflammation, Cochin Institute, INSERM U1016, CNRS UMR8104, Paris Descartes University, Paris, France.
Yonatan
Y
Ganor
Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel.
Ran
R
Cohen
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Department of Neurology, Assaf Harofeh Medical Center, Zriffin, Israel.
Lea
L
Pollak
Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel.
Vivian
V
Teichberg
School of Behavioral Sciences, Academic College of Tel Aviv-Yaffo, Tel Aviv, Israel. Electronic address: mialevite@mta.ac.il.
Mia
M
Levite
D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000097:blood*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003072:Cognition Disorders / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D004827:Epilepsy / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D001523:Mental Disorders / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D018091:Receptors, AMPA / Q000276:immunology*; D012189:Retrospective Studies; D055815:Young Adult
D000906:Antibodies; D018091:Receptors, AMPA; C104723:glutamate receptor ionotropic, AMPA 3
Behavioral psychiatric abnormalities; Epilepsy; GluR3 antibodies; GluR3B; Glutamate AMPA receptors