PMID- 23196492
OWN - NLM
STAT- MEDLINE
DCOM- 20140421
LR  - 20190918
IS  - 1882-0654 (Electronic)
IS  - 0009-918X (Linking)
VI  - 52
IP  - 11
DP  - 2012
TI  - [Clinical profiles of Japanese patients with anti-NMDAR encephalitis and 
      functional analysis of the anti-NMDAR antibodies].
PG  - 985-7
AB  - The N-methyl-D-aspartate receptor (NMDAR) encephalitis is characterized by a set 
      of neurologic and psychiatric symptoms including seizures. Early removal of the 
      antibodies ameliorate the disease course and the antibodies are thought to relate 
      closely to its symptoms. We tested the anti-NMDAR antibodies with cell-based 
      assay using NMDAR NR1/NR2 heteromers expressed on HEK cells and found 41 
      antibody-positive cases from 2008 to 2011. Most of them showed typical clinical 
      features as described, however, some show schizophrenia-like symptoms or chronic 
      epilepsy. The NMDAR is essential both for memory and synaptic plasticity, most 
      notably expressed as long-term potentiation (LTP). The binding of antibody is 
      shown to dimerize NMDARs and trigger their internalization on the postsynaptic 
      site, thereby suppressing NMDAR-mediated transmission. Despite such molecular 
      understanding, it is not known whether the antibody-mediated dysfunction of 
      NMDARs underlies the symptoms of the anti-NMDAR encephalitis. We tested whether 
      the disease-produced antibodies suppress NMDAR-dependent LTP induction, and found 
      the CSF positive for anti-NMDAR antibodies suppressed induction of LTP at CA1 
      synapses in mouse hippocampal slices. Antibody absorption with NR1 antigens 
      reversed the suppression of LTP, confirming that anti-NMDAR antibodies 
      specifically suppressed LTP. The present experiments firmly support the proposal 
      that the anti-NMDAR antibody is responsible for cognitive disorders like amnesia 
      accompanying with this disease.
FAU - Tanaka, Keiko
AU  - Tanaka K
AD  - Department of Neurology, Medical Research Institute, Kanazawa Medical University.
LA  - jpn
PT  - English Abstract
PT  - Journal Article
PL  - Japan
TA  - Rinsho Shinkeigaku
JT  - Rinsho shinkeigaku = Clinical neurology
JID - 0417466
RN  - 0 (Autoantibodies)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Anti-N-Methyl-D-Aspartate Receptor Encephalitis/*immunology
MH  - Autoantibodies/*immunology
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - Humans
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Receptors, N-Methyl-D-Aspartate/*immunology
EDAT- 2012/12/01 06:00
MHDA- 2014/04/22 06:00
CRDT- 2012/12/01 06:00
PHST- 2012/12/01 06:00 [entrez]
PHST- 2012/12/01 06:00 [pubmed]
PHST- 2014/04/22 06:00 [medline]
AID - DN/JST.JSTAGE/clinicalneurol/52.985 [pii]
AID - 10.5692/clinicalneurol.52.985 [doi]
PST - ppublish
SO  - Rinsho Shinkeigaku. 2012;52(11):985-7. doi: 10.5692/clinicalneurol.52.985.