PMID- 33466431
OWN - NLM
STAT- MEDLINE
DCOM- 20210623
LR  - 20210623
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 10
IP  - 1
DP  - 2021 Jan 5
TI  - NMDA and AMPA Receptor Autoantibodies in Brain Disorders: From Molecular 
      Mechanisms to Clinical Features.
LID - 10.3390/cells10010077 [doi]
LID - 77
AB  - The role of autoimmunity in central nervous system (CNS) disorders is rapidly 
      expanding. In the last twenty years, different types of autoantibodies targeting 
      subunits of ionotropic glutamate receptors have been found in a variety of 
      patients affected by brain disorders. Several of these antibodies are directed 
      against NMDA receptors (NMDAR), mostly in autoimmune encephalitis, whereas a 
      growing field of research has identified antibodies against AMPA receptor (AMPAR) 
      subunits in patients with different types of epilepsy or frontotemporal dementia. 
      Several in vitro and in vivo studies performed in the last decade have 
      dramatically improved our understanding of the molecular and functional effects 
      induced by both NMDAR and AMPAR autoantibodies at the excitatory glutamatergic 
      synapse and, consequently, their possible role in the onset of clinical symptoms. 
      In particular, the method by which autoantibodies can modulate the localization 
      at synapses of specific target subunits leading to functional impairments and 
      behavioral alterations has been well addressed in animal studies. Overall, these 
      preclinical studies have opened new avenues for the development of novel 
      pharmacological treatments specifically targeting the synaptic activation of 
      ionotropic glutamate receptors.
FAU - Gardoni, Fabrizio
AU  - Gardoni F
AD  - Department of Pharmacological and Biomolecular Sciences, University of Milan, 
      20133 Milan, Italy.
FAU - Stanic, Jennifer
AU  - Stanic J
AUID- ORCID: 0000-0003-1295-4568
AD  - Department of Pharmacological and Biomolecular Sciences, University of Milan, 
      20133 Milan, Italy.
FAU - Scheggia, Diego
AU  - Scheggia D
AUID- ORCID: 0000-0003-2586-9717
AD  - Department of Pharmacological and Biomolecular Sciences, University of Milan, 
      20133 Milan, Italy.
FAU - Benussi, Alberto
AU  - Benussi A
AUID- ORCID: 0000-0002-8703-6940
AD  - Neurology Unit, Centre for Neurodegenerative Disorders, Department of Clinical 
      and Experimental Sciences, University of Brescia, 25123 Brescia, Italy.
FAU - Borroni, Barbara
AU  - Borroni B
AUID- ORCID: 0000-0001-9340-9814
AD  - Neurology Unit, Centre for Neurodegenerative Disorders, Department of Clinical 
      and Experimental Sciences, University of Brescia, 25123 Brescia, Italy.
FAU - Di Luca, Monica
AU  - Di Luca M
AD  - Department of Pharmacological and Biomolecular Sciences, University of Milan, 
      20133 Milan, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210105
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
RN  - 0 (Autoantibodies)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Autoantibodies/*immunology
MH  - Epilepsy/*immunology/pathology
MH  - Frontotemporal Dementia/*immunology/pathology
MH  - Humans
MH  - Receptors, AMPA/*immunology
MH  - Receptors, N-Methyl-D-Aspartate/*immunology
MH  - Synapses/*immunology
PMC - PMC7824909
OTO - NOTNLM
OT  - autoimmunity
OT  - brain disorders
OT  - excitatory synapse
OT  - glutamate
COIS- The authors declare no conflict of interest.
EDAT- 2021/01/21 06:00
MHDA- 2021/06/24 06:00
PMCR- 2021/01/05
CRDT- 2021/01/20 01:06
PHST- 2020/12/16 00:00 [received]
PHST- 2020/12/29 00:00 [revised]
PHST- 2021/01/04 00:00 [accepted]
PHST- 2021/01/20 01:06 [entrez]
PHST- 2021/01/21 06:00 [pubmed]
PHST- 2021/06/24 06:00 [medline]
PHST- 2021/01/05 00:00 [pmc-release]
AID - cells10010077 [pii]
AID - cells-10-00077 [pii]
AID - 10.3390/cells10010077 [doi]
PST - epublish
SO  - Cells. 2021 Jan 5;10(1):77. doi: 10.3390/cells10010077.