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Brain Behav Immun. 2017 Nov;66:125-134. doi: 10.1016/j.bbi.2017.07.011. Epub 2017 Jul 18.

Synapsin-antibodies in psychiatric and neurological disorders: Prevalence and clinical findings.

Author information

1
Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany. Electronic address: markus.hoeltje@charite.de.
2
Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany. Electronic address: robert.mertens@charite.de.
3
St. Olav's Hospital, Trondheim University Hospital, Department of Psychiatry, Trondheim, Norway; Norwegian University of Science and Technology, Faculty of Medicine and Health Science, Department of Mental Health, Trondheim, Norway. Electronic address: morten.b.schou@ntnu.no.
4
St. Olav's Hospital, Trondheim University Hospital, Department of Psychiatry, Trondheim, Norway; Norwegian University of Science and Technology, Faculty of Medicine and Health Science, Department of Mental Health, Trondheim, Norway. Electronic address: sverrege@gmail.com.
5
Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany. Electronic address: elena.kochova@gmail.com.
6
Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Germany. Electronic address: sven.jarius@med.uni-heidelberg.de.
7
Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany; German Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany. Electronic address: harald.pruess@charite.de.
8
Institute for Experimental Immunology, Affiliated to Euroimmun AG, Lübeck, Germany. Electronic address: l.komorowski@euroimmun.de.
9
Institute for Experimental Immunology, Affiliated to Euroimmun AG, Lübeck, Germany. Electronic address: c.probst@euroimmun.de.
10
Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany; Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Germany. Electronic address: friedemann.paul@charite.de.
11
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany; Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Germany. Electronic address: judith.bellmann-strobl@charite.de.
12
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Electronic address: gitler@bgu.ac.il.
13
Center for Synaptic Neuroscience and Technology, Istituto Italiano di Tecnologia, Genova, Italy. Electronic address: Fabio.Benfenati@iit.it.
14
Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany; Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Electronic address: johannes.piepgras@charite.de.
15
Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany. Electronic address: Gudrun.ahnert@charite.de.
16
Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Electronic address: klemens.ruprecht@charite.de.

Abstract

OBJECTIVE:

To study the prevalence of autoantibodies to synapsin in patients with psychiatric and neurological disorders and to describe clinical findings in synapsin antibody positive patients.

METHODS:

Sera of 375 patients with different psychiatric and neurological disorders and sera of 97 healthy controls were screened (dilution 1:320) for anti-synapsin IgG using HEK293 cells transfected with rat synapsin Ia. Positive sera were further analyzed by immunoblots with brain tissue from wild type and synapsin knock out mice and with HEK293 cells transfected with human synapsin Ia and Ib. Binding of synapsin IgG positive sera to primary neurons was studied using murine hippocampal neurons.

RESULTS:

IgG in serum from 23 (6.1%) of 375 patients, but from none of the 97 healthy controls (p=0.007), bound to rat synapsin Ia transfected cells with a median (range) titer of 1:1000 (1:320-1:100,000). Twelve of the 23 positive sera reacted with a protein of the molecular size of synapsin I in immunoblots of wild type but not of synapsin knock out mouse brain tissue. Out of 19/23 positive sera available for testing, 13 bound to human synapsin Ia and 16 to human synapsin Ib transfected cells. Synapsin IgG positive sera stained fixed and permeabilized murine hippocampal neurons. Synapsin IgG positive patients had various psychiatric and neurological disorders. Tumors were documented in 2 patients (melanoma, small cell lung carcinoma); concomitant anti-neuronal or other autoantibodies were present in 8 patients.

CONCLUSIONS:

Autoantibodies to human synapsin Ia and Ib are detectable in a proportion of sera from patients with different psychiatric and neurological disorders, warranting further investigation into the potential pathophysiological relevance of these antibodies.

KEYWORDS:

Antibodies; Autoimmunity; Demyelinating disease; Neurologic disorders; Psychiatric disorders; Serum; Synapsin

PMID:
28733081
DOI:
10.1016/j.bbi.2017.07.011
[Indexed for MEDLINE]

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