Antonietta Gentile

TL;DR: Light is shed on the connection between inflammation and synaptopathy in MS and EAE, which sheds light not only on the pathophysiology of MS but also on that of primary neurodegenerative disorders in which inflammatory processes contribute to disease progression.

TL;DR: Current evidence of the role of IL-1β and TNF in the regulation of synaptic strength at both physiological and pathological levels are introduced and discussed, in particular speculating on their involvement in the synaptic plasticity changes observed in the EAE brain.

TL;DR: In EAE mice, significant alterations of synaptic plasticity rules in the hippocampus were found and microglial activation in the EAE hippocampus was associated with IL-1β expression, and hippocampal slices from control mice incubated with activated microglia displayed alterations of GABAergic transmission similar to those seen in EAE brains.

TL;DR: Results show that siponimod has neuroprotective effects in the CNS of EAE mice, which are likely independent of its peripheral immune effect, suggesting that this drug could be effective in limiting neurodegenerative pathological processes in MS.

TL;DR: The results highlight the crucial role played by the proinflammatory IL-1β in triggering molecular and synaptic events involved in neurodegenerative processes that characterize neuroinflammatory diseases such as MS.