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News and Articles
Scientists at University of Ferrara publish research in epilepsy
June 29, 2009
According to recent research from Ferrara, Italy, "A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis)." "Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis," wrote B. Paradiso and colleagues, University of Ferrara (see also Epilepsy). The researchers concluded: "It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences." Paradiso and colleagues published their study in Proceedings of the National Academy of Sciences of the United States of America (Localized delivery of fibroblast growth factor-2 and brain-derived neurotrophic factor reduces spontaneous seizures in an epilepsy model. Proceedings of the National Academy of Sciences of the United States of America, 2009;106(17):7191-7196). For additional information, contact M. Simonato, University of Ferrara, Pharmacology Sect, Dept. of Clinic & Experimental Medical, I-44100 Ferrara, Italy. Publisher contact information for the journal Proceedings of the National Academy of Sciences of the United States of America is: National Acad Sciences, 2101 Constitution Avenue NW, Washington, DC 20418, USA.
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