The frequency of inflammatory episodes in the early stages of multiple sclerosis (MS) has been correlated with late neurodegeneration, but the mechanism by which inflammation gives rise to delayed neuronal damage is unknown. Increased activity of the neurotransmitter glutamate is thought to play a role in the inflammation-driven neurodegenerative process of MS, and therefore we tested whether inflammatory cytokines released during acute MS attacks have the property of enhancing glutamate-mediated transmission and excitotoxicity in central neurons.
Rossi, S., Furlan, R., De Chiara, V., Motta, C., Studer, V., Mori, F., et al. (2012). Interleukin-1β causes synaptic hyperexcitability in multiple sclerosis. ANNALS OF NEUROLOGY, 71(1), 76-83 [10.1002/ana.22512].
Interleukin-1β causes synaptic hyperexcitability in multiple sclerosis
ROSSI, SILVIA;MORI, FRANCESCO;BERNARDI, GIORGIO;CENTONZE, DIEGO
2012-01-01
Abstract
The frequency of inflammatory episodes in the early stages of multiple sclerosis (MS) has been correlated with late neurodegeneration, but the mechanism by which inflammation gives rise to delayed neuronal damage is unknown. Increased activity of the neurotransmitter glutamate is thought to play a role in the inflammation-driven neurodegenerative process of MS, and therefore we tested whether inflammatory cytokines released during acute MS attacks have the property of enhancing glutamate-mediated transmission and excitotoxicity in central neurons.| File | Dimensione | Formato | |
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2012_Rossi_Interleukin-1b Causes Synaptic Hyperexcitability in Multiple Sclerosis.pdf
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