Publications by authors named "S F Lichtenthaler"
Despite numerous studies on fetal therapy for myelomeningoceles (MMC), the pathophysiology of this malformation remains poorly understood. This study aimed to analyze the biochemical profile and proteome of amniotic fluid (AF) supernatants from MMC fetuses to explore the prenatal pathophysiology. Biochemical analysis of 61 AF samples from MMC fetuses was compared with 45 healthy fetuses' samples.
View Article and Find Full Text PDFBackground: The prion-like spreading of Tau pathology is the leading cause of disease progression in various tauopathies. A critical step in propagating pathologic Tau in the brain is the transport from the extracellular environment and accumulation inside naïve neurons. Current research indicates that human neurons internalize both the physiological extracellular Tau (eTau) monomers and the pathological eTau aggregates.
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- * In studies using a mouse model lacking the NPC1 protein in immune cells, researchers found significant changes in microglial lipid profiles, increased microglial activity, and symptoms resembling NPC disease, such as lifespan reduction and motor issues.
- * Monitoring translocator protein (TSPO) levels in the blood may be useful for assessing NPC disease progression and treatment response, as shown by changes in TSPO levels following a specific therapy that appeared beneficial for patients.
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- * Research identified that levels of Lingo2, a protein linked to excitatory synapse formation, were increased in neurons from the VPA model, suggesting its role as an excitatory synapse organizer.
- * The secreted form of Lingo2 (sLingo2) was found to enhance excitatory synapses in both mouse and human neurons, indicating that better understanding sLingo2's mechanisms could shed light on the development of ASD.
Loss-of-function mutations in CLN3 cause juvenile Batten disease, featuring neurodegeneration and early-stage neuroinflammation. How loss of CLN3 function leads to early neuroinflammation is not yet understood. Here, we have comprehensively studied microglia from Cln3 mice, a genetically accurate disease model.
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