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Zeitschrift für Psychologie ; 231(2):137-148, 2023.
Article in English | CINAHL | ID: covidwho-20237143

ABSTRACT

Adverse experiences interact with individual vulnerability in the etiology of mental disorders, but due to the paucity of longitudinal studies, their precise interplay remains unclear. Here, we investigated how individual differences in threat responsiveness modulated adjustments in negative affect during the COVID-19 pandemic. Participants (N = 441) underwent a fear conditioning and generalization experiment between 2013 and 2020 and were reassessed regarding anxiety and depression symptoms after the pandemic outbreak. Participants showed increased levels of negative affect following pandemic onset, which were partly modulated by laboratory measures of threat responsiveness. Decreased differentiation of threat and safety signals in participants with higher prepandemic depression and anxiety scores in the laboratory assessment were most predictive of increased symptom levels after the onset of the pandemic. However, effects were small and should be replicated in independent samples to further characterize how individual differences in threat processing interact with adverse experiences in the development of psychopathology.

3.
Biol Psychiatry ; 92(4): 261-274, 2022 08 15.
Article in English | MEDLINE | ID: covidwho-2122338

ABSTRACT

BACKGROUND: Autoimmune psychosis may be caused by well-characterized anti-neuronal autoantibodies, such as those against the NMDA receptor. However, the presence of additional anti-central nervous system (CNS) autoantibodies in these patients has not been systematically assessed. METHODS: Serum and cerebrospinal fluid (CSF) from patients with schizophreniform and affective syndromes were analyzed for immunoglobulin G anti-CNS autoantibodies using tissue-based assays with indirect immunofluorescence on unfixed murine brain tissue as part of an extended routine clinical practice. After an initial assessment of patients with red flags for autoimmune psychosis (n = 30), tissue-based testing was extended to a routine procedure (n = 89). RESULTS: Based on the findings from all 119 patients, anti-CNS immunoglobulin G autoantibodies against brain tissue were detected in 18% (n = 22) of patients (serum 9%, CSF 18%) following five principal patterns: 1) against vascular structures, most likely endothelial cells (serum 3%, CSF 8%); 2) against granule cells in the cerebellum and/or hippocampus (serum 4%, CSF 6%); 3) against myelinated fibers (serum 2%, CSF 2%); 4) against cerebellar Purkinje cells (serum 0%, CSF 2%); and 5) against astrocytes (serum 1%, CSF 1%). The patients with novel anti-CNS autoantibodies showed increased albumin quotients (p = .026) and white matter changes (p = .020) more frequently than those who tested negative for autoantibodies. CONCLUSIONS: The study demonstrates five novel autoantibody-binding patterns on brain tissue of patients with schizophreniform and affective syndromes. CSF yielded positive findings more frequently than serum analysis. The frequency and spectrum of autoantibodies in these patient groups may be broader than previously thought.


Subject(s)
Autoantibodies , Endothelial Cells , Animals , Brain , Granulocyte-Macrophage Colony-Stimulating Factor , Humans , Immunoglobulin G , Mice , Mood Disorders
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