Biomarkers of neurodegeneration in neural autoantibody-associated psychiatric syndromes: A retrospective cohort study.

Autoimmunity Neural autoantibody Neurodegeneration Neurodegenerative biomarkers Psychiatric syndrome

Journal

Journal of translational autoimmunity
ISSN: 2589-9090
Titre abrégé: J Transl Autoimmun
Pays: Netherlands
ID NLM: 101759413

Informations de publication

Date de publication:
2022
Historique:
received: 23 08 2022
revised: 01 10 2022
accepted: 03 10 2022
entrez: 14 10 2022
pubmed: 15 10 2022
medline: 15 10 2022
Statut: epublish

Résumé

Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. Several lines of evidence suggest that neurodegenerative processes are involved here. We are investigating whether autoantibody-positive psychiatric syndromes differ from those that are autoantibody-negative in cerebrospinal fluid (CSF) neurodegeneration markers. We retrospectively analyzed data from 167 psychiatric patients at the University Medical Center Göttingen from 2017 to 2020. We divided this patient cohort into two, namely antibody-positive and antibody-negative. We compared various clinical features, neurodegeneration markers, and their autoantibody status in CSF and serum. We then compared both cohorts' neurodegeneration markers to a representative Alzheimer cohort. We subdivided the patients into their diverse psychiatric syndromes according to the manual to assess and document psychopathology in psychiatry (the AMDP), and compared the neurodegeneration markers. Antibody-associated psychiatric syndromes do not appear to reveal significantly greater neurodegeneration than their antibody-negative psychiatric syndromes. 71% of antibody-positive patients fulfilled the criteria for a possible and 22% for a definitive autoimmune encephalitis. Our autoantibody-positive patient cohort's relative risk to develop an possible autoimmune encephalitis was 9%. We also noted that phosphorylated tau protein 181 (ptau 181) did not significantly differ between antibody-associated psychiatric syndromes and our Alzheimer cohort. The psycho-organic syndrome usually exhibits the most prominent neurodegeneration markers, both in antibody-positive and antibody-negative psychiatric patients. We did not find hints for neurodegenerative processes in our antibody-positive versus AD cohort considering total tau or amyloid markers. However, our findings indicate that the neurodegeneration marker ptau181 does not differ significantly between antibody-positive and Alzheimer cohorts, further suggesting axonal neurodegeneration in antibody-positive patients as AD patients have an elevated ptau181. The evidence we uncovered thus suggests that axonal neurodegeneration might affect patients suffering from autoantibody-associated psychiatric syndromes.

Sections du résumé

Background UNASSIGNED
Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. Several lines of evidence suggest that neurodegenerative processes are involved here. We are investigating whether autoantibody-positive psychiatric syndromes differ from those that are autoantibody-negative in cerebrospinal fluid (CSF) neurodegeneration markers.
Methods UNASSIGNED
We retrospectively analyzed data from 167 psychiatric patients at the University Medical Center Göttingen from 2017 to 2020. We divided this patient cohort into two, namely antibody-positive and antibody-negative. We compared various clinical features, neurodegeneration markers, and their autoantibody status in CSF and serum. We then compared both cohorts' neurodegeneration markers to a representative Alzheimer cohort. We subdivided the patients into their diverse psychiatric syndromes according to the manual to assess and document psychopathology in psychiatry (the AMDP), and compared the neurodegeneration markers.
Results UNASSIGNED
Antibody-associated psychiatric syndromes do not appear to reveal significantly greater neurodegeneration than their antibody-negative psychiatric syndromes. 71% of antibody-positive patients fulfilled the criteria for a possible and 22% for a definitive autoimmune encephalitis. Our autoantibody-positive patient cohort's relative risk to develop an possible autoimmune encephalitis was 9%. We also noted that phosphorylated tau protein 181 (ptau 181) did not significantly differ between antibody-associated psychiatric syndromes and our Alzheimer cohort. The psycho-organic syndrome usually exhibits the most prominent neurodegeneration markers, both in antibody-positive and antibody-negative psychiatric patients.
Discussion UNASSIGNED
We did not find hints for neurodegenerative processes in our antibody-positive versus AD cohort considering total tau or amyloid markers. However, our findings indicate that the neurodegeneration marker ptau181 does not differ significantly between antibody-positive and Alzheimer cohorts, further suggesting axonal neurodegeneration in antibody-positive patients as AD patients have an elevated ptau181. The evidence we uncovered thus suggests that axonal neurodegeneration might affect patients suffering from autoantibody-associated psychiatric syndromes.

Identifiants

pubmed: 36238527
doi: 10.1016/j.jtauto.2022.100169
pii: S2589-9090(22)00030-2
pmc: PMC9550648
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100169

Informations de copyright

© 2022 The Authors.

Déclaration de conflit d'intérêts

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Références

Alzheimers Dement. 2018 Apr;14(4):535-562
pubmed: 29653606
Pharmacopsychiatry. 1986 Mar;19(2):55-7
pubmed: 3703923
Neurol Neuroimmunol Neuroinflamm. 2020 Mar 13;7(3):
pubmed: 32170044
J Neural Transm (Vienna). 2021 Mar;128(3):357-369
pubmed: 33677623
Front Immunol. 2022 Mar 03;13:837376
pubmed: 35309366
Nat Rev Immunol. 2021 Dec;21(12):798-813
pubmed: 33976421
Ther Adv Neurol Disord. 2021 Mar 19;14:1756286421998906
pubmed: 33796145
Front Neurol. 2022 Jun 16;13:879009
pubmed: 35785337
Continuum (Minneap Minn). 2019 Feb;25(1):14-33
pubmed: 30707185
J Transl Autoimmun. 2022 Sep 21;5:100165
pubmed: 36176328
Lancet Neurol. 2016 Apr;15(4):391-404
pubmed: 26906964
Front Psychiatry. 2022 Jan 28;12:778684
pubmed: 35153852
Ann Clin Transl Neurol. 2014 Oct;1(10):822-32
pubmed: 25493273
Lancet Neurol. 2008 Dec;7(12):1091-8
pubmed: 18851928
Curr Opin Immunol. 2019 Aug;59:115-120
pubmed: 31430650
Brain Sci. 2021 Dec 23;12(1):
pubmed: 35053759
Geriatr Gerontol Int. 2018 Sep;18(9):1350-1355
pubmed: 30044040
Eur J Neurol. 2016 Apr;23(4):796-806
pubmed: 26822123
Neurology. 2017 Oct 3;89(14):1471-1475
pubmed: 28878050
Brain Behav Immun Health. 2020 Oct 01;9:100154
pubmed: 34589896
Transl Psychiatry. 2021 Sep 13;11(1):474
pubmed: 34518517
Brain. 2012 May;135(Pt 5):1622-38
pubmed: 22539258
Psychol Med. 2020 Sep 07;:1-12
pubmed: 32892761
Front Psychiatry. 2017 Feb 16;8:25
pubmed: 28261116
Arch Psychiatr Nervenkr (1970). 1983;233(3):223-45
pubmed: 6615188
Front Psychiatry. 2020 Jul 03;11:576
pubmed: 32714214
Front Psychiatry. 2022 May 30;13:864769
pubmed: 35711589
Dement Geriatr Cogn Disord. 2021;50(2):153-160
pubmed: 34237731
Brain Behav Immun. 2021 Aug;96:106-112
pubmed: 34022370
Cells. 2021 Apr 08;10(4):
pubmed: 33917676
Front Neurol. 2021 Jul 02;12:673347
pubmed: 34276536
Neurology. 2021 May 18;96(20):e2546-e2557
pubmed: 33795390
Front Neurol. 2018 Sep 19;9:668
pubmed: 30283395
Int J Mol Sci. 2020 Jul 13;21(14):
pubmed: 32668637
Neurol Clin. 1998 Feb;16(1):83-105
pubmed: 9421542

Auteurs

Aaron Levin Juhl (AL)

Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Translational Psychoneuroscience, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.

Insa Maria Grenzer (IM)

Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Translational Psychoneuroscience, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.

Bianca Teegen (B)

Clinical Immunological Laboratory Prof. Stöcker, Groß Grönau, Germany.

Jens Wiltfang (J)

Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
German Center for Neurodegenerative Diseases (DZNE), Von-Siebold-Str. 3a, 37075, Göttingen, Germany.
Neurosciences and Signaling Group, Institute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.

Dirk Fitzner (D)

Department of Neurology, University Medical Center Göttingen, Robert-Koch Straße 40, 37075, Göttingen, Germany.

Niels Hansen (N)

Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Translational Psychoneuroscience, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.

Classifications MeSH