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
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
100169Informations 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.
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