Publications by authors named "Helene Jamann"
Amyloid-peptide (Aβ) monomeric forms (ABM) occurring in presymptomatic Alzheimer's disease (AD) brain are thought to be devoid of neurotoxicity while the transition/aggregation of ABM into oligomers is determinant for Aβ-induced toxicity since Aβ is predominantly monomeric up to 3 µM and aggregates over this concentration. However, recent imaging and/or histopathological investigations revealed alterations of myelin in prodromal AD brain in absence of aggregated Aβ oligomers, suggesting that ABM may induce toxicity in myelin-producing cells in early AD-stages. To check this hypothesis, here we studied ABM effects on the viability of the Human oligodendrocyte cell line (HOG), a reliable oligodendrocyte model producing myelin proteins.
View Article and Find Full Text PDFArticle Synopsis
- Multiple sclerosis (MS) is an autoimmune disease that damages myelin in the central nervous system, leading to injury of brain and spinal cord cells due to immune cell infiltration, particularly by pro-inflammatory Th17 cells.
- The study investigated how these Th17 cells interact with oligodendrocytes (the myelin-producing cells) through specific adhesion molecules, finding that the presence of certain molecules like ALCAM helps these cells adhere, which can lead to cell death.
- Results showed that in the presence of inflammatory cytokines or activated T cells, the expression of MCAM decreased, offering protective insights that targeting ALCAM could reduce harmful interactions between Th17 cells and oligodendrocytes, potentially leading to new therapeutic strategies for
Article Synopsis
- The study examines the role of inflammation in drug-resistant epilepsy (DRE) and evaluates how two new anti-epileptic drugs (AEDs), brivaracetam and lacosamide, affect immune cell activation.
- Research shows that both AEDs do not negatively impact the survival or activation of immune cells at lower doses, but higher doses reduce CD8 T cell proliferation and certain markers.
- Although these AEDs do not delay the onset of experimental autoimmune encephalomyelitis (EAE), they improve the disease's clinical course, suggesting they may help reduce neuroaxonal damage in DRE.
Article Synopsis
- GM-CSF plays a significant role in chronic inflammatory diseases like multiple sclerosis (MS) by affecting myeloid cell functions, specifically monocyte-derived macrophages (MDMs) and microglia.
- The study found that GM-CSF increases IL-15 expression in MDMs from both healthy individuals and MS patients, as well as in human microglia, which may enhance the immune response against MS.
- Notably, while GM-CSF-stimulated MDMs elevate CD8 T lymphocytes' production of effector molecules, this enhancement occurs independently of IL-15, suggesting that GM-CSF influences myeloid cells through multiple pathways.
Article Synopsis
- The CRISPR-Cas9 system has transformed the creation of genetically engineered animal models, particularly conditional alleles, which are complex due to the need for precise genome modifications using two guides.
- Researchers developed a modified sequential electroporation method that successfully produced conditional allele mouse models for eight different genes using two approaches: consecutive and non-consecutive electroporation.
- The results showed varying targeting efficiencies, with both strategies yielding successful models that could enhance the generation of conditional allele models in future research.
Article Synopsis
- Multiple sclerosis (MS) involves damage to myelin and oligodendrocytes (cells that produce myelin) in the central nervous system, with Th17 cells being particularly harmful to these OLs.
- Research utilized live imaging and single-cell RNA sequencing to show that Th17 cells interact more aggressively with OLs than Th2 cells, leading to the production of pro-inflammatory molecules and increased cell death.
- The study confirmed that granzyme B, which is secreted by Th17 cells during direct contact, contributes to oligodendrocyte death, illustrating a critical mechanism in MS progression.
Early multiple sclerosis lesions feature relative preservation of oligodendrocyte cell bodies with dying back retraction of their myelinating processes. Cell loss occurs with disease progression. Putative injury mediators include metabolic stress (low glucose/nutrient), pro-inflammatory mediators (interferon γ and tumour necrosis factor α), and excitotoxins (glutamate).
View Article and Find Full Text PDFObjective: Myelin regeneration in the human central nervous system relies on progenitor cells within the tissue parenchyma, with possible contribution from previously myelinating oligodendrocytes (OLs). In multiple sclerosis, a demyelinating disorder, variables affecting remyelination efficiency include age, severity of initial injury, and progenitor cell properties. Our aim was to investigate the effects of age and differentiation on the myelination potential of human OL lineage cells.
View Article and Find Full Text PDFPro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.
Proc Natl Acad Sci U S A
August 2021
T helper (Th)17 cells are considered to contribute to inflammatory mechanisms in diseases such as multiple sclerosis (MS). However, the discussion persists regarding their true role in patients. Here, we visualized central nervous system (CNS) inflammatory processes in models of MS live in vivo and in MS brains and discovered that CNS-infiltrating Th17 cells form prolonged stable contact with oligodendrocytes.
View Article and Find Full Text PDFDysregulated immune profiles have been described in symptomatic patients infected with SARS-CoV-2. Whether the reported immune alterations are specific to SARS-CoV-2 infection or also triggered by other acute illnesses remains unclear. We performed flow cytometry analysis on fresh peripheral blood from a consecutive cohort of (a) patients hospitalized with acute SARS-CoV-2 infection, (b) patients of comparable age and sex hospitalized for another acute disease (SARS-CoV-2 negative), and (c) healthy controls.
View Article and Find Full Text PDFIn Alzheimer's disease (AD), tau, a microtubule-associated protein (MAP), becomes hyperphosphorylated, aggregates, and accumulates in the somato-dendritic compartment of neurons. In parallel to its intracellular accumulation in AD, tau is also released in the extracellular space, as revealed by its increased presence in cerebrospinal fluid (CSF). Consistent with this, recent studies, including ours, have reported that neurons secrete tau, and several therapeutic strategies aim to prevent the intracellular tau accumulation.
View Article and Find Full Text PDFObjective: Adult drug-resistant epilepsy (DRE) is associated with significant morbidity. Infiltration of immune cells is observed in DRE epileptic foci; however, the relation between DRE and the peripheral immune cell compartment remains only partially understood. We aimed to investigate differences in immune cell populations, cytokines, and neurodegenerative biomarkers in the peripheral blood of subjects with epilepsy versus healthy controls, and in DRE compared to well-controlled epilepsy (WCE).
View Article and Find Full Text PDF