Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures
By M. Maroso, S. Balosso, T. Ravizza, J. Liu, Eleonora Aronica, A. Iyer, C. Rossetti, M. Molteni, Maura Casalgrandi, A. Manfredi and 2 more. Nature Medicine, 2010
897 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/f85a32c9ef370bc73b7696deb6fd6fcba48814e6
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Immunology
In Oncology
Citations in the corpus
- HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4 (2012, background): “Rage / BM cells were incubated for 30 min in the presence or absence of 10 µg/ml LPS-Rs before performing chemotaxis assay.”
- The treatment of super-refractory status epilepticus: a critical review of available therapies and a clinical treatment protocol. (2011, background): “The second development has been the increasing evidence that inflammation plays an important role in epileptogenesis, and especially the activation of specific inflammatory signalling pathways such as the interleukin-1 receptor/toll-like receptor (IL-1R/ TLR) pathway, both experimentally and in huma”
- Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “…et al., 1999; Viviani et al., 2003), or the secretion of HMGB1 (a damage-associated molecular pattern that is secreted by hyperexcited or damaged neurons and possibly glia) (Maroso et al., 2010) activate known signal transduction pathways that induce neuronal hyper-excitability and epilepsy.”
- Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer’s disease model (2012, result): “An alternative interpretation of our results is that synaptic, network, cognitive, and behavioral dysfunctions result from parallel processes triggered by a similar upstream mechanism that is blocked by LEV, for example, glutamate spillover leading to overactivation of extrasynaptic NMDA receptors, ”
- Microglia activation triggers astrocyte-mediated modulation of excitatory neurotransmission (2011, background): “The expression of TLR4 has occasionally been detected in astrocytes and neurons under pathological conditions (62, 66).”