Publications by authors named "Ramona Gerhards"

Article Synopsis
  • Neurodegeneration is a significant factor in neurologic disorders linked to GAD65 antibodies, and this study explores neuroaxonal damage's relationship with disease duration and clinical symptoms.
  • In a study involving 50 patients, serum neurofilament light chain (sNfL) levels were measured and correlated with disease progression and clinical presentations, using MRI to assess brain structure changes.
  • The findings show elevated sNfL levels early in the disease, especially in patients with cerebellar ataxia and limbic encephalitis, alongside atrophy in specific brain regions, highlighting the importance of early intervention in these conditions.
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  • Researchers have identified autoantibodies against myelin oligodendrocyte glycoprotein (MOG) as a key factor in a new disease called MOG-antibody-associated disease (MOGAD), which resembles multiple sclerosis.
  • The study explores how these MOG-specific antibodies damage the nervous system, focusing on the roles of complement proteins and Fc-receptors.
  • Findings show that both mechanisms contribute equally to nerve damage, while the activation of certain immune cells in the brain depends specifically on FcR interactions, suggesting potential targets for new treatments.
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  • Some COVID-19 patients retain specific IgG antibodies for over 6 months, but others may lose them after that period.
  • Research on 17 patients showed that even those who lost IgG still had persistent SARS-CoV-2-specific B cells, which are essential for long-term immunity.
  • Antibodies from these B cells were effective in neutralizing the virus and showed varying levels of response to different virus variants, suggesting that monitoring B cells could be a better method for assessing past infections than just measuring serum antibodies.
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  • * The research showed that the N-terminal part of MOG alone is insufficient for ELISA-based identification of MOG antibodies in patients, indicating that full-length MOG is required for effective antibody binding.
  • * The intracellular part of MOG is crucial in maintaining optimal spacing for bivalent binding of antibodies, highlighting the necessity of a cell-based approach for identifying MOG-Abs in patients.
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Article Synopsis
  • Autoimmune disorders of the central nervous system (CNS) are diverse, and understanding the specific autoantigens is crucial for improving therapy and understanding disease causes.
  • Researchers studied oligodendrocyte myelin glycoprotein (OMGP) as a potential autoimmune target and found autoantibodies to OMGP in a small percentage of multiple sclerosis patients, a child with encephalomyelitis, and one patient with psychosis, but not in healthy controls.
  • The presence of OMGP-specific T cells in an animal model led to a new type of experimental autoimmune encephalomyelitis characterized by unusual inflammation, emphasizing the role of OMGP in patient diagnostic and therapeutic stratification.
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  • The study aimed to identify circulating MOG-specific B cells in the blood of patients with MOG antibodies and investigate their relationship with serum anti-MOG antibody levels and epitope specificity.
  • Researchers analyzed blood samples from 21 MOG-antibody-positive patients and 26 controls, finding that a higher frequency of MOG-specific B cells was present in patients, but only about 60% of them tested positive for these B cells.
  • The findings suggest that the quantity of circulating MOG-specific B cells varies significantly among patients and does not correlate with serum MOG antibody levels, indicating potential differences in the sources of these antibodies, which could inform future patient-specific treatments.
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High levels of antibodies against glutamic acid decarboxylase (GAD) are observed in patients with different neurological disorders, but cells producing these autoantibodies are largely unexplored. We detect circulating GAD-reactive B cells in peripheral blood that readily differentiate into antibody-producing cells. These cells are highly elevated in most patients with GAD-antibody-associated disorders (n = 15) compared to controls (n = 19).

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Objective: Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) occur in a proportion of patients with inflammatory demyelinating diseases of the central nervous system (CNS). We analyzed their pathogenic activity by affinity-purifying these antibodies (Abs) from patients and transferring them to experimental animals.

Methods: Patients with Abs to MOG were identified by cell-based assay.

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The formation of neuronal circuits is a key process of development, laying foundations for behavior. The cellular mechanisms regulating circuit development are not fully understood. Here, we reveal Psidin as an intracellular regulator of Drosophila olfactory system formation.

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