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Francesca De Vito

Researcher at University of Rome Tor Vergata

Publications -  39
Citations -  1507

Francesca De Vito is an academic researcher from University of Rome Tor Vergata. The author has contributed to research in topics: Multiple sclerosis & Experimental autoimmune encephalomyelitis. The author has an hindex of 17, co-authored 31 publications receiving 1033 citations. Previous affiliations of Francesca De Vito include Sapienza University of Rome.

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Synaptopathy connects inflammation and neurodegeneration in multiple sclerosis

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.
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Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation

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.
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Stress induces region specific alterations in microRNAs expression in mice.

TL;DR: The data suggest that control of mRNA translation through miRs is an additional mechanism by which stressful events regulates protein expression in the frontal cortex.
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Siponimod (BAF312) prevents synaptic neurodegeneration in experimental multiple sclerosis.

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.
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Interleukin-1β Alters Glutamate Transmission at Purkinje Cell Synapses in a Mouse Model of Multiple Sclerosis

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.