Publications by authors named "Nils Mein"
Article Synopsis
- Microglia are crucial immune cells in the brain that help regulate brain development, synaptic plasticity, and neuronal networks, but may contribute to synaptic loss during diseases.
- A study assessed the effects of long-term and short-term microglia depletion on dendritic spine density, finding long-term depletion increased spine density, whereas short-term depletion with repopulation led to decreased spine density and excitatory neurotransmission.
- Long-term microglia depletion shows potential as a treatment for diseases with harmful microglial activity, but repopulation appears to worsen synaptic health, suggesting ongoing regulation of microglial activity might be a better strategy.
Background: Sepsis-associated encephalopathy (SAE) is characterized by symptoms of delirium including hallucinations, impaired concentration, agitation, or coma and is associated with poor outcome in the early phase of sepsis. In addition, sepsis survivors often suffer from persisting memory deficits and impaired executive functions. Recent studies provide evidence that microglia are involved in the pathophysiology of SAE.
View Article and Find Full Text PDFSepsis-associated encephalopathy (SAE) is a severe and frequent complication of sepsis causing delirium, coma, and long-term cognitive dysfunction. We identified microglia and C1q complement activation in hippocampal autopsy tissue of patients with sepsis and increased C1q-mediated synaptic pruning in a murine polymicrobial sepsis model. Unbiased transcriptomics of hippocampal tissue and isolated microglia derived from septic mice revealed an involvement of the innate immune system, complement activation, and up-regulation of lysosomal pathways during SAE in parallel to neuronal and synaptic damage.
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